Epithelial-mesenchymal transition (EMT) is important for tumor metastasis. Detection of EMT protein expression and observation of morphological changes are commonly used to identify EMT. Diffusion-weighted magnetic resonance imaging (DW-MRI) and measuring apparent diffusion coefficient (ADC) values are noninvasive techniques for characterizing tumor microenvironments. We investigated the difference in ADC values between epithelial- and mesenchymal-like subcutaneous mouse xenografted tumors using DW-MRI. Epithelial-like MM189 PB-Klf4 and BL322 PB-Klf4 cells were generated from tumor suppressive Kruppel-like factor 4 (Klf4)-expressing mesenchymal-like MM189 and BL322 cells. The ADC values of xenografted tumors from epithelial-like MM189 PB-Klf4 and BL322 PB-Klf4 were significantly lower than those from their mesenchymal-like counterparts (p < 0.05 and p < 0.01, respectively). Our results suggested that DW-MRI is a potential tool for observing mesenchymal- or epithelial-like characteristics of

TY - JOUR. T1 - Regulation of epithelial-mesenchymal transition in breast cancer cells by cell contact and adhesion. AU - Cichon, Magdalena A.. AU - Nelson, Celeste M.. AU - Radisky, Derek C. PY - 2015/2/9. Y1 - 2015/2/9. N2 - Epithelial-mesenchymal transition (EMT) is a physiological program that is activated during cancer cell invasion and metastasis. We show here that EMT-related processes are linked to a broad and conserved program of transcriptional alterations that are influenced by cell contact and adhesion. Using cultured human breast cancer and mouse mammary epithelial cells, we find that reduced cell density, conditions under which cell contact is reduced, leads to reduced expression of genes associated with mammary epithelial cell differentiation and increased expression of genes associated with breast cancer. We further find that treatment of cells with matrix metalloproteinase-3 (MMP-3), an inducer of EMT, interrupts a defined subset of cell contact-regulated genes, including genes ...

To address the impact of cellular origin on acute myeloid leukemia (AML), we generated an inducible transgenic mouse model for MLL-AF9-driven leukemia. MLL-AF9 expression in long-term hematopoietic stem cells (LT-HSC) in vitro resulted in dispersed clonogenic growth and expression of genes involved in migration and invasion. In vivo, 20% LT-HSC-derived AML were particularly aggressive with extensive tissue infiltration, chemoresistance, and expressed genes related to epithelial-mesenchymal transition (EMT) in solid cancers. Knockdown of the EMT regulator ZEB1 significantly reduced leukemic blast invasion. By classifying mouse and human leukemias according to Evi1/EVI1 and Erg/ERG expression, reflecting aggressiveness and cell of origin, and performing comparative transcriptomics, we identified several EMT-related genes that were significantly associated with poor overall survival of AML patients.

TY - JOUR. T1 - M2 macrophage polarization modulates epithelial-mesenchymal transition in cisplatin-induced tubulointerstitial fibrosis. AU - Yu, Chia Cherng. AU - Chien, Chiang Ting. AU - Chang, Tzu Ching. PY - 2016/3/1. Y1 - 2016/3/1. N2 - Cisplatin-induced nephrotoxicity leaded to apoptosis of tubular epithelial cells (ECs) and tubulointerstitial fibrosis through ROS stress and inflammatory cytokines. Tubulointerstitial fibrosis caused by cisplatin might be via activation of resident fibroblasts and epithelial-mesenchymal transition (EMT) of tubular ECs. Inflammatory niche was crucial for progression of fibroblast activation or EMT. It had been reported that M1/M2 macrophage polarization regulated pro-inflammation or pro-resolving phase in damage repairing. However, the role of macrophage polarization on cisplatin-induced EMT of tubular ECs had not been well elucidated. In this study, we used co-cultured cell model and condition medium to examine the interaction between tubular ECs, ...

TY - JOUR. T1 - MiR-5003-3p promotes epithelial-mesenchymal transition in breast cancer cells through Snail stabilization and direct targeting of E-cadherin. AU - Kwak, Seo Young. AU - Yoo, Je Ok. AU - An, Hyun Ju. AU - Bae, In Hwa. AU - Park, Myung Jin. AU - Kim, Joon. AU - Han, Young Hoon. N1 - Publisher Copyright: © The Author (2016). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, IBCB, SIBS, CAS. Copyright: Copyright 2017 Elsevier B.V., All rights reserved.. PY - 2016/10/1. Y1 - 2016/10/1. N2 - One of the initial steps in metastatic dissemination is the epithelial-mesenchymal transition (EMT). Along this line, microRNAs (miRNAs) have been shown to function as important regulators of tumor progression at various stages. Therefore, we performed a functional screening for EMT-regulating miRNAs and identified several candidate miRNAs. Among these, we demonstrated that miR-5003-3p induces cellular features characteristic of EMT. miR-5003-3p induced ...

TY - JOUR. T1 - Essential role for Smad3 in angiotensin II-induced tubular epithelial-mesenchymal transition. AU - Yang, Fuye. AU - Huang, Xiao Ru. AU - Chung, Arthur C K. AU - Hou, Chun Cheng. AU - Lai, Kar Neng. AU - Lan, Hui Yao. PY - 2010/8. Y1 - 2010/8. N2 - Angiotensin II (Ang II) is a key mediator of chronic kidney disease, in which epithelial-mesenchymal transition (EMT) is a critical process mediated by the TGFβ/Smad signalling pathway. The present study examined the specific role of Smads in Ang II-induced EMT in vitro and in vivo. We found that Ang II signalled through the receptor of AT1, not AT2, to activate Smad2/3 and induce EMT in a normal rat tubular epithelial cell line (NRK52E). Activation of Smads by Ang II was attributed to degradation of an inhibitory Smad7, which was mediated by the AT1-Smurf2-dependent ubiquitin degradation mechanism because blockade of AT1 receptor or knockdown of Smurf2 inhibited Smad7 loss, thereby reducing Smad2/3 activation and EMT in response to ...

Epithelial-mesenchymal transition (EMT) is implicated in the pathogenesis of lung fibrosis and cancer metastasis, two conditions associated with cigarette smoke (CS). H358 PA-824 cells cultured in RPMI-1640 medium with 1% fetal bovine serum. Pretreatment with N-acetylcysteine (NAC), a potent antioxidant and precursor of glutathione, abrogated changes in these EMT markers. In addition, CSE activated Src kinase (shown as increased phosphorylation of Src at Tyr418) and the Src kinase inhibitor, PP2, inhibited CS-stimulated EMT changes, suggesting that Src is critical in CSE-stimulated EMT induction. Furthermore, NAC treatment abrogated CSE-stimulated Src activation. However, co-incubation with catalase had no effect on CSE-mediated Src activation. Finally, acrolein, an unsaturated aldehyde present in CSE, caused Src activation. Taken together, these data suggest that CSE initiates EMT through Src, which is activated by CS through redox modification. models are obviously required to confirm current ...

Malignant progression in cancer requires populations of tumor-initiating cells (TICs) endowed with unlimited self renewal, survival under stress, and establishment of distant metastases. Additionally, the acquisition of invasive properties driven by epithelial-mesenchymal transition (EMT) is critical for the evolution of neoplastic cells into fully metastatic populations. Here, we characterize 2 human cellular models derived from prostate and bladder cancer cell lines to better understand the relationship between TIC and EMT programs in local invasiveness and distant metastasis. The model tumor subpopulations that expressed a strong epithelial gene program were enriched in highly metastatic TICs, while a second subpopulation with stable mesenchymal traits was impoverished in TICs. Constitutive overexpression of the transcription factor Snai1 in the epithelial/ TIC-enriched populations engaged a mesenchymal gene program and suppressed their self renewal and metastatic phenotypes. Conversely, ...

During progression of melanoma, malignant melanocytes can be reprogrammed into mesenchymal-like cells through a process similar to epithelial-mesenchymal transition (EMT), which is associated with downregulation of the junctional protein E-cadherin and acquisition of a migratory phenotype. Recent evidence supports a role for SLUG, a transcriptional repressor of E-cadherin, as a melanocyte lineage transcription factor that predisposes to melanoma metastasis. However, the signals responsible for SLUG expression in melanoma are unclear and its role in the invasive phenotype is not fully elucidated. Here, we report that SLUG expression and activation is driven by SPARC (also known as osteonectin), a secreted extracellular matrix-associated factor that promotes EMT-like changes. Ectopic expression or knockdown of SPARC resulted in increased or reduced expression of SLUG, respectively. SLUG increase occurred concomitantly with SPARC-mediated downregulation of E-cadherin and P-cadherin, and induction ...

BACKGROUND: Epithelial-mesenchymal transition (EMT) plays a crucial role in circulating tumor cells (CTCs) dissemination and cancer metastasis. OBJECTIVE: To investigate the EMT phenotypes of CTCs in hepatocellular carcinoma (HCC) patients and the cl

Our data indicate that a major proportion of CTC of metastatic breast cancer patients shows EMT and tumor stem cell characteristics. Further studies are needed to prove whether these markers might serve as an indicator for therapy resistant tumor cell populations and, therefore, an inferior prognosi …

Full Text - Increasing studies have indicated that circular RNAs (circRNAs) are important in cancer progression. However, few circRNAs associated with epithelial-mesenchymal transition (EMT) have been elucidated in esophageal squamous cell carcinoma (ESCC). In this study, we aimed to identify whether hsa_circ_0006948 promotes ESCC cell EMT and explore its biological mechanisms. We first screened circRNA expression profiles using a circRNA microarray, and found that the expression of a novel circRNA, hsa_circ_0006948, is increased in 153 ESCC tissues and cell lines compared with noncancerous tissues and cell lines. Additionally, high hsa_circ_0006948 levels were positively associated with lymphatic metastasis and poor prognosis. Functionally, the assays indicated that cell proliferation, migration and invasion were promoted by hsa_circ_0006948 both in vitro and in vivo. Furthermore, we analyzed the relationship between hsa_circ_0006948 and miR-490-3p through bioinformatics, luciferase reporter assays,

Epithelial mesenchymal transition (EMT) has long been associated with breast cancer cell invasiveness and evidence of EMT processes in clinical samples is growing rapidly. Genome-wide transcriptional profiling of increasingly larger numbers of human breast cancer (HBC) cell lines have confirmed the …

We read with interest the recent review article by Bartis et al in Thorax1 and a similar one from some of the same authors in European Respiratory Review,2 addressing the potential importance of epithelial mesenchymal transition (EMT) in lung development and disease. We would like to take issue with the approach used, which is to emphasise molecular patterns potentially associated with EMT, rather than starting with any empiric evidence that EMT is present as an active pathological process.. EMT has been differentiated into three different types.3 It is a vital process during embryogenesis (type 1 EMT), but can also be induced as a result of persistent epithelial stimulation leading to organ fibrosis (type 2 EMT). In COPD, this could be responsible for destruction of small airways. Epithelial stimulation can also lead to malignancy, through type 3 EMT, that is, EMT plus angiogenesis, which we have documented in large airway.3. The major criteria for recognising EMT activity in vivo were ...

Introduction Bovine papillomavirus (BPV) is the etiological agent of bovine papillomatosis, infectious and neoplastic disease, characterized by the presence of multiple papillomas that can regress spontaneously or to persist and progress to malignancies when in association with environmental cofactors. Although recognized that the BPV can induce DNA damages, the viral role following cancer initiation remains unresolved. Based on this, we stablished cell lines derived from cutaneous papilloma, fibropapilloma and esophageal carcinoma to study the BPV action on epithelial-mesenchymal transition (EMT). Our results showed strong evidences that the virus action can contribute to EMT and, therefore, metastasis. Aim In this study, we analyzed the expression levels of the EMT markers (cytokeratin 10, STAT3 Y705, Oct-3/4 and vimentin) in paraffin-embed samples, using the same tissues that originated the cell lines previous studied, aiming to validate the results observed using cell lines. Material and Methods

Epithelial-to-mesenchymal transition (EMT) of peritoneal mesothelial cells is a pathological process that occurs during peritoneal dialysis. EMT leads to peritoneal fibrosis, ultrafiltration failure and eventually to the discontinuation of therapy. Signaling pathways involved in mesothelial EMT are thus of great interest, but are mostly unknown. We used primary mesothelial cells from human omentum to analyze the role of the p38 MAPK signaling pathway in the induction of EMT. The use of specific inhibitors, a dominant-negative p38 mutant and lentiviral silencing of p38α demonstrated that p38 promotes E-cadherin expression both in untreated cells and in cells co-stimulated with the EMT-inducing stimuli transforming growth factor (TGF)-β1 and interleukin (IL)-1β. p38 inhibition also led to disorganization and downregulation of cytokeratin filaments and zonula occludens (ZO)-1, whereas expression of vimentin was increased. Analysis of transcription factors that repress E-cadherin expression ...

Metastasis is the leading cause of cancer related deaths and yet there are no targeted therapies for metastatic cancers. Epithelial-mesenchymal transition (EMT) promotes metastasis by inducing invasive properties in epithelial tumors. Although EMT-mediated cellular and molecular changes are well understood, very little is known about EMT-induced metabolic changes. To determine whether EMT induces metabolic alterations, HER2-positive BT-474 breast cancer cells were induced to undergo a stable EMT using mammosphere culture, as previously described by us for the ERα-positive MCF-7 breast cancer cells. Two epithelial breast cancer cell lines (BT-474 and MCF-7) were compared to their respective EMT-derived mesenchymal progeny (BT-474EMT and MCF-7EMT) for changes in metabolic pathways including glycolysis, glycogen metabolism, pentosephosphate pathway, hexosamine biosynthetic pathway, serine biosynthetic pathway, de novolipogenesis pathway and gluconeogenesis. Both EMT-derived breast cancer cells displayed

There is increasing evidence that the presence of CTCs and DTCs is correlated with minimal residual disease or disease progression in patients with breast cancer. Nevertheless, the underlying molecular characteristics of micrometastatic cells associated with the development of overt metastases remain largely unknown. EMT is a multistep process that has been suggested to play a key role in cancer progression and metastasis [12]. Accordingly, CTCs bearing characteristics of an EMT phenotype should be actively involved in tumour dissemination, proliferation and metastasis. Twist is a transcription factor that, among others, participates in EMT and is upregulated in many tumour cells [18-22, 47]. In a recent report by Watson et al. [24], Twist expression was specifically enhanced in a gene signature obtained from epithelial cell adhesion molecule-enriched bone marrow samples of patients with breast cancer after neoadjuvant chemotherapy. Twist also increases VEGF expression, while it is directly ...

This study highlights the clinical implications of preoperative serum NRDC measurements in patients with ICC, which may contribute to the identification of patients with a poor prognosis. OS and DFS were significantly stratified by serum NRDC levels in the primary (development) and validation cohorts. The expression levels of NRDC in sera and cancerous tissues were significantly linked; therefore, an evaluation of pathophysiologic features in resected tissues provided an insight into the clinical significance of serum NRDC. NRDC mRNA levels correlated with EMT-related genes in primary tumors. Moreover, direct correlations were observed between serum NRDC and mRNA levels of major EMT-TF, suggesting that serum NRDC has potential as a surrogate marker for EMT features in primary tumors. This hypothesis was supported by a cell analysis because the gene silencing of NRDC in ICC cell lines reduced EMT-related gene expression. Functionally, the gene KD of NRDC was accompanied by attenuated ...

Puisieux et al. discuss endothelial to mesenchymal transition (EMT)-inducing transcription factors in tumorigenesis. They explore how EMT contributes not only to tumour progression through its roles in invasion and metastasis, but also to malignant transformation and early tumour development by impinging on tumour suppressive pathways and cell differentiation states. The plasticity of cancer cells underlies their capacity to adapt to the selective pressures they encounter during tumour development. Aberrant reactivation of epithelial-mesenchymal transition (EMT), an essential embryonic process, can promote cancer cell plasticity and fuel both tumour initiation and metastatic spread. Here we discuss the roles of EMT-inducing transcription factors in creating a pro-tumorigenic setting characterized by an intrinsic ability to withstand oncogenic insults through the mitigation of p53-dependent oncosuppressive functions and the gain of stemness-related properties.

Pancreatic acinar cells acquire in vitro a pancreatic progenitor phenotype associated with activation of p53, growth arrest and senescence. A similar program is also activated in chronic pancreatitis. To assess the mechanisms involved in this process, we cultured pancreatic acinar cells from wild-type, p53 (-/-) , p16 (-/-) and p21 (-/-) mice. Cultures from p53 (-/-) mice, but not those from p16 (-/-) or p21 (-/-) mice, display an enhanced proliferation and can be expanded continuously for more than 20 passages. p53 (-/-) cells also display features of stemness such as enhanced sphere formation, increased expression of pancreatic multipotent progenitor markers (Ptf1a, Pdx1, Cpa1, c-myc, Sox9 and Hnf1b), and of the stemness regulators Bmi1 and Klf4. Upon subculture, p53 (-/-) cells undergo an epithelial-mesenchymal transition (EMT) and express high levels of vimentin and of the transcriptional regulators Snai1, Snai2, Twist, Zeb1 and Zeb2. Genetic lineage tracing unequivocally demonstrates the epithelial

Polysialic acid (PSA) is highly expressed during embryonic development, but barely expressed during postnatal development, and may be re-expressed in cancer tissues. In this study, motility and migration assays were performed to compare the changes in cell behavior between non-malignant and maligant cells. Next, the expression levels of PSA were evaluated in 4 human and mouse normal breast or breast cancer (BC) cell lines using 1,2-diamino-4,5-methylenedioxybenzene-labeling HPLC technology, as well as in human clinical BC tissue samples. PSA expression was significantly higher in malignant cells (where it appeared to facilitate cell migration and motility) than in non-malignant cells. Enhanced PSA expression levels were also observed during epithelial-mesenchymal transition (EMT), a leading cause of cancer cell metastasis, which was induced in the NMuMG and MCF10A cells by treatment with transforming growth factor-β1 (TGF-β1). An increased PSA expression also correlated with the disease stage in the

Epithelial-mesenchymal transitions (EMTs) drive the generation of cell diversity during both evolution and development. More and more evidence has pointed to a model where EMT is not a binary switch but a reversible process that can be stabilized at intermediate states. Despite our vast knowledge on the signaling pathways that trigger EMT, we know very little about how EMT happens in a step-wise manner. Live imaging of cells that are undergoing EMT in intact, living, animals will provide us valuable insights into how EMT is executed at both the cellular and molecular levels and help us identify and understand the intermediate states. Here, we describe how to image early stages of EMT in the mesoderm cells of live Drosophila melanogaster embryos and how to image contractile myosin that suspends EMT progression.

The development of the human kidney is a complex process requiring interactions between epithelial and mesenchymal cells. The condensed cap mesenchyme is hypothesized to generate a population of stem/progenitor cells that undergo mesenchymal-epithelial transition (MET) originating nephrons. Few immunohistochemical markers are available for detecting cap mesenchymal cells in the early phases of MET. METHODS: The expression of MUC1 was evaluated in the kidneys, of 4 human foetuses and 2 newborns. RESULTS: MUC1 immunoreactivity was detected in all the examined kidneys in the cap mesenchyme and in the renal vesicles. Immunostaining for MUC1 in cap mesenchymal cells changed from one nodule to the next: some mesenchymal nodules were negative, some showed MUC1 reactivity in scattered cells, whereas in others, positive cells revealed the presence of a roundish developing epithelial structure. CONCLUSIONS: Our data clearly indicates, for the first time to the best of our knowledge, immunohistochemical ...

The overall survival of patients with hepatocellular carcinoma (HCC) remains poor, and the molecular pathogenesis remains incompletely defined in HCC. Here we report that increased expression of αB-Crystallin in human HCC predicts poor survival and disease recurrence after surgery. Multivariate analysis identifies αB-Crystallin expression as an independent predictor for postoperative recurrence and overall survival. We show that elevated expression of αB-Crystallin promotes HCC progression in vivo and in vitro. We demonstrate that αB-Crystallin overexpression fosters HCC progression by inducing epithelial-mesenchymal transition (EMT) in HCC cells through activation of the extracellular-regulated protein kinase (ERK) cascade, which can counteract the effect of sorafenib. αB-Crystallin complexes with and elevates 14-3-3ζ protein, leading to up-regulation of ERK1/2 activity. Moreover, overexpression of αB-Crystallin in HCC cells induces EMT progression through an ERK1/2/Fra-1/slug signaling ...

In this study, we investigated the effects of p63 modulation in epithelial plasticity in human keratinocytes. The p63 isoforms ΔNp63α, ΔNp63β, and ΔNp63γ were ectopically expressed in normal human epidermal keratinocytes (NHEKs). The epithelial or mesenchymal state was determined by morphological changes and altered expression of various markers, e.g. fibronectin, E-Cadherin, and keratin 14. Overexpression of ΔNp63α and ΔNp63β but not ΔNp63γ isoforms led to morphological changes consistent with epithelial-mesenchymal transition (EMT). However, only ΔNp63α overexpression was able to maintain the morphological changes and molecular phenotype consistent with EMT. Interestingly, knockdown of all p63 isoforms by transfection of p63 siRNA also led to the EMT phenotype, further confirming the role of p63 in regulating the epithelial phenotype in NHEKs. EMT in NHKs accompanied loss of Grainyhead-Like 2 (GHRL2) and miR-200 family gene expression, both of which play crucial roles in ...

Li, H, et al. (2017) The EMT regulator ZEB2 is a novel dependency of human and murine acute myeloid leukemia. Blood. 2017 Jan 26; 129(4):497-508. PM ID: ...

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TY - JOUR. T1 - L-carnitine via PPARγ- and Sirt1-dependent mechanisms attenuates epithelial-mesenchymal transition and renal fibrosis caused by perfluorooctanesulfonate. AU - Chou, Hsiu Chu. AU - Wen, Li Li. AU - Chang, Chih Cheng. AU - Lin, Chien Yu. AU - Jin, Lu. AU - Juan, Shu Hui. PY - 2017/12/1. Y1 - 2017/12/1. N2 - We have previously reported that perfluorooctanesulfonate (PFOS) causes cell apoptosis in renal tubular epithelial cells (RTCs). Here, we extend our findings and provide evidence of epithelial-mesenchymal transition (EMT)-associated renal fibrosis caused by PFOS and the protection by L-carnitine. Our results demonstrate that PFOS increased the expression of EMT and renal injury biomarkers (eg, N-cadherin, vimentin, Snail, Kim1, and Lcn2). In addition, PFOS caused EMT induction through Sirt1-mediated PPARγ deacetylation and inactivation. L-carnitine reversed the EMT induction caused by PFOS and alleviated PFOS-mediated increases in cellmigration by reactivating PPARγ through ...

TY - JOUR. T1 - Sirtuins and Cancer. T2 - Role in the Epithelial-Mesenchymal Transition. AU - Palmirotta, Raffaele. AU - Cives, Mauro. AU - Della-Morte, David. AU - Capuani, Barbara. AU - Lauro, Davide. AU - Guadagni, Fiorella. AU - Silvestris, Franco. PY - 2016. Y1 - 2016. N2 - The human sirtuins (SIRT1-SIRT7) enzymes are a highly conserved family of NAD+-dependent histone deacetylases, which play a critical role in the regulation of a large number of metabolic pathways involved in stress response and aging. Cancer is an age-Associated disease, and sirtuins may have a considerable impact on a plethora of processes that regulate tumorigenesis. In particular, growing evidence suggests that sirtuins may modulate epithelial plasticity by inducing transcriptional reprogramming leading to epithelial-mesenchymal transition (EMT), invasion, and metastases. Though commonly regarded as EMT inducers, sirtuins may also suppress this process, and their functional properties seem to largely depend on the ...

OBJECTIVE: In papillary thyroid carcinoma (PTC), while the role of BRAF is well established, the contribution of BRAF to epithelial-mesenchymal transition is not. STUDY DESIGN/SETTING: To elucidate the relationship between BRAF, surrogates of epithelial-mesenchymal transition (Snail, E-cadherin) and established histopathologic prognosticators in papillary thyroid carcinoma. SUBJECTS/METHODS: In this IRB approved cross-sectional study, 50 cases of archived annotated PTC samples were retrieved and immunohistochemically stained for Snail and E-cadherin protein. A semi-quantitative scoring system (incorporating proportion and intensity) was utilized. RESULTS: Snail and E-cadherin expression were noted in 44% and 84% of BRAF mutant and, in 29% and 95% of BRAFWT samples, respectively. No statistically significant correlations were noted between Snail, E-cadherin and histopathologic prognosticators. However, a trend was noted between Snail expression and tumor size | 5 cm (P=0.07). Statistically significant

Epithelial-mesenchymal transition (EMT) contributes to the progression and metastasis of cancer cells and is associated with a more invasive phenotype of cancer. The Wnt/β-catenin signaling pathway is one of the major pathways involved in EMT regulation. Many studies provide evidence that β-catenin, the key regulator of the canonical Wnt signaling pathway, is important in regulating EMT in cancer. However, the roles of Wnt3a, the representative canonical Wnt ligand, in EMT and colon cancer progression have not yet been fully explored. The expression levels of Wnt3a and EMT-associated proteins (E-cadherin, vimentin, and β-catenin) were assessed by immunohistochemistry in human colon cancer tissues to evaluate the clinicopathological significance of Wnt3a, as well as the correlation between Wnt3a and EMT. We then upregulated Wnt3a expression in HCT116 colon cancer cells, established a nude mouse xenograft model, detected the expression of EMT and Wnt/β-catenin signaling-associated proteins, and

MicroRNAs (miRNAs) are reported to function as a major component in the cellular signaling circuit, which regulates epithelial‑mesenchymal transition (EMT). Dysregulation of the microRNA‑200 (miR‑200) family and EMT‑associated genes enables tumor metastasis and resistance to therapy. The present study profiled miR‑200 family members miR‑200a, miR‑200b, miR‑200c, miR‑141 and miR‑429, and also several EMT‑regulatory genes including zinc finger E‑box‑binding homeobox (ZEB)1, ZEB2, epithelial cadherin and vimentin in 40 oral primary tumors in order to understand their role(s) in oral squamous cell carcinoma (OSCC). The reverse transcription‑quantitative polymerase chain reaction was used to analyze each sample. Results demonstrated a significant downregulation of miR‑200 family members in tumors with a history of tobacco chewing/smoking ( ...

Epithelial-mesenchymal transition (EMT) is normally one particular mechanism of possessed resistance to inhibitors of the skin growth factor receptor-tyrosine kinases (EGFR-TKIs) in non-small cell lung cancer (NSCLC). micro-RNA-200c, which can regulate ZEB1 adversely, was decreased in HCC4006EUr cells significantly. Our outcomes recommend that elevated can get EMT-related obtained level of resistance to EGFR-TKIs in NSCLC. Tries should end up being produced to explore concentrating on to resensitize TKI-resistant tumors. Launch Despite the advantage of skin development aspect receptor-tyrosine kinase inhibitors (EGFR-TKIs) in non-small cell lung cancers (NSCLC) sufferers with mutation [1], obtained level of resistance to these therapies is normally a vital scientific issue. Although the Testosterone levels790M supplementary mutation [2] and gene amplification [3] may jointly accounts for 70% of this level of resistance, systems for the staying 30% are unsure. The epithelial-mesenchymal ...

Hotair is a member of the recently described class of noncoding RNAs called lincRNA (large intergenic noncoding RNA). Various studies suggest that Hotair acts regulating epigenetic states by recruiting chromatin-modifying complexes to specific target sequences that ultimately leads to suppression of several genes. Although Hotair has been associated with metastasis and poor prognosis in different tumor types, a deep characterization of its functions in cancer is still needed. Here, we investigated the role of Hotair in the scenario of epithelial-to-mesenchymal transition (EMT) and in the arising and maintenance of cancer stem cells (CSCs). We found that treatment with TGF-1 resulted in increased Hotair expression and triggered the EMT program. Interestingly, ablation of Hotair expression by siRNA prevented the EMT program stimulated by TGF-1, and also the colony-forming capacity of colon and breast cancer cells. Furthermore, we observed that the colon CSC subpopulation (CD133(+)/CD44(+)) ...

Background Accumulating studies show that epithelial-mesenchymal changeover (EMT) plays a part in tumor metastasis. of leptin on breasts cancer tumor cells was examined. Besides a range of pathway inhibitors aswell as RNA disturbance concentrating on pyruvate kinase M2 (PKM2) had been utilized to clarify the root system of leptin-mediated EMT in vitro and in vivo. Outcomes The results showed that leptin marketed breasts cancer tumor cells EMT visibly turned on the PI3K/AKT signaling pathway and upregulated PKM2 appearance. An antibody against the leptin receptor (anti-ObR) as well as the PI3K/AKT signaling pathway inhibitor LY294002 considerably abolished leptin-induced PKM2 appearance and EMT-associated marker appearance. SiRNA targeting PKM2 abolished leptin-induced migration invasion and EMT-associated marker appearance partially. In vivo xenograft tests indicated that RNA disturbance against PKM2 suppressed breasts cancer tumor metastasis and development. Conclusions Our data claim that ...

Background Accumulating studies show that epithelial-mesenchymal changeover (EMT) plays a part in tumor metastasis. of leptin on breasts cancer tumor cells was examined. Besides a range of pathway inhibitors aswell as RNA disturbance concentrating on pyruvate kinase M2 (PKM2) had been utilized to clarify the root system of leptin-mediated EMT in vitro and in vivo. Outcomes The results showed that leptin marketed breasts cancer tumor cells EMT visibly turned on the PI3K/AKT signaling pathway and upregulated PKM2 appearance. An antibody against the leptin receptor (anti-ObR) as well as the PI3K/AKT signaling pathway inhibitor LY294002 considerably abolished leptin-induced PKM2 appearance and EMT-associated marker appearance. SiRNA targeting PKM2 abolished leptin-induced migration invasion and EMT-associated marker appearance partially. In vivo xenograft tests indicated that RNA disturbance against PKM2 suppressed breasts cancer tumor metastasis and development. Conclusions Our data claim that ...

Insulin-like growth factor I (IGF-I) can induce epithelial mesenchymal transition (EMT) in many epithelial tumors; however, the molecular mechanism by which this occurs is not clearly understood. Additionally, little is known about the involvement of IGF-I in gastric cancer. Two gastric cancer cell lines were treated with IGF-I to induce EMT and levels of transcription factor ZEB2 and microRNA-200c (miR-200c) were measured. Cells were treated with Akt/ERK inhibitors to investigate the role of these pathways in IGF-I-mediated EMT. Transfection of shRNA plasmids was used to silence the ubiquitin ligase Cbl-b to assess its involvement in this process. The relationship between IGF-IR and Cbl-b expression, and the effect of IGF-IR and Cbl-b on metastasis were analyzed in primary gastric adenocarcinoma patients. IGF-I-induced gastric cancer cell EMT was accompanied by ZEB2 up-regulation. Furthermore, both Akt/ERK inhibitors and knockdown of Akt/ERK gene reversed IGF-I-induced ZEB2 up-regulation and EMT

AIM: To evaluate the effects of epidermal growth factor (EGF) on transforming growth factor-beta1 (TGF- 1)-induced epithelial-mesenchymal transition (EMT) in human corneal epithelial cells (HCECs). METHODS: HCECs were cultured and treated with TGF- 1 for establishing the model of EMT in vitro. Biological effect of EGF on TGF- 1-induced EMT was evaluated. Proteins and mRNAs expression changes of E-cadherin, N-cadherin and Fibronectin (EMT-relative markers) after TGF- 1 or TGF- 1 combined EGF treatment were detected by Western blot and RT-PCR, respectively. Viability and migration of HCECs were measured by CCK-8, transwell cell migration assay and cell scratch wound healing assay. Activation of Smad2, ERK, p38, JNK and Akt signaling pathways were evaluated by Western blot. Inhibitors of relevant signaling pathways were added to the HCECs to explore the key signal mechanism. RESULTS: With treatment of TGF- 1 only, three EMT-relative proteins and mRNA expression showed that EMT up-regulated in a

TY - JOUR. T1 - Sox9 mediates Notch1-induced mesenchymal features in lung adenocarcinoma. AU - Capaccione, Kathleen M.. AU - Hong, Xuehui. AU - Morgan, Katherine M.. AU - Liu, Wenyu. AU - Bishop, Michael J.. AU - Liu, Lian Xin. AU - Markert, Elke. AU - Deen, Malik. AU - Minerowicz, Christine. AU - Allen, Thaddeus. AU - Pine, Sharon R.. PY - 2014. Y1 - 2014. N2 - Sox9 has gained increasing importance both functionally and as a prognostic factor in cancer. We demonstrate a functional role for Sox9 in inducing a mesenchymal phenotype in lung ADC. We show that Sox9 mRNA and protein are overexpressed in lung ADC, particularly those with KRAS mutations. Sox9 expression correlated with the Notch target gene Hes1, and numerous other Notch pathway components. We observed that Sox9 is a potent inducer of lung cancer cell motility and invasion, and a negative regulator of E-cadherin, a key protein that is lost during epithelialmesenchymal transition (EMT). Moreover, we show that Notch1 signaling directly ...

Purpose.: MicroRNA-181a (miR-181a) is thought to be involved in posterior capsule opacification (PCO). This study investigated the role of miR-181a in the proliferation, migration, and epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs). Methods.: The expression of miR-181a was detected in human PCO-attached LECs and LECs obtained from patients with anterior polar cataracts by quantitative RT-PCR (qRT-PCR). The proliferation of SRA01/04 cells transfected with miR-181a mimics was analyzed by MTT assays and bromodeoxyuridine (BrdU)-incorporation assays. The migration of SRA01/04 cells was evaluated by wound-healing assays and Transwell migration. Luciferase reporter assays were used to validate the regulation of a putative target of miR-181a. Results.: The expression of miR-181a is decreased in human PCO-attached LECs and LECs obtained from patients with anterior polar cataracts. A significant decrease in proliferation was observed in SRA01/04 cells transfected with miR-181a ...

OBJECTIVE The aim of this study was to investigate the role of SOX10 in NPC and the underlying molecular mechanisms. METHODS Expression of SOX10 was initially assessed in human NPC tissues and a series of NPC cell lines through quantitative real-time PCR (qRT-PCR) and western blot. Then, cell proliferation, cycle, migration and invasion of NPC cells with knockdown of SOX10 were examined by MTT, flow cytometry, transwell migration and invasion assay, respectively. Finally, nude mice tumorigenicity experiments were performed to evaluate the effects of SOX10 on NPC growth and metastasis in vivo. RESULTS SOX10 was significantly increased in NPC tissues and cell lines. In vitro experiments revealed that loss of SOX10 obviously inhibited cell proliferation, migration and invasion, as well as epithelial-mesenchymal transition (EMT) process in NPC cells. In vivo experiments further demonstrated that disrupted SOX10 expression restrained NPC growth and metastasis, especially in lung and liver. CONCLUSION

The self-renewal capacity ascribed to embryonic stem cells (ESC) is reminiscent of cancer cell proliferation, raising speculation that a common network of genes may regulate these traits. A search for general regulators of these traits yielded a set of microRNAs for which expression is highly enriched in human ESCs and liver cancer cells (HCC) but attenuated in differentiated quiescent hepatocytes. Here, we show that these microRNAs promote hESC self-renewal, as well as HCC proliferation, and when overexpressed in normally quiescent hepatocytes, induce proliferation and activate cancer signaling pathways. Proliferation in hepatocytes is mediated through translational repression of Pten, Tgfbr2, Klf11, and Cdkn1a, which collectively dysregulates the PI3K/AKT/mTOR and TGFβ tumor suppressor signaling pathways. Furthermore, aberrant expression of these miRNAs is observed in human liver tumor tissues and induces epithelial-mesenchymal transition in hepatocytes. These findings suggest that microRNAs ...

Metastasis, not the primary tumor, is responsible for the majority of breast cancer-related deaths. Emerging evidence indicates that breast cancer stem cells (CSCs) and the epithelial-to-mesenchymal transition (EMT) cooperate to produce circulating tumor cells (CTCs) that are highly competent for metastasis. CTCs with both CSC and EMT characteristics have recently been identified in the bloodstream of patients with metastatic disease. Breast CSCs have elevated tumorigenicity required for metastatic outgrowth, while EMT may promote CSC character and endows breast cancer cells with enhanced invasive and migratory potential. Both CSCs and EMT are associated with a more flexible cytoskeleton and with anoikis-resistance, which help breast carcinoma cells survive in circulation. Suspended breast carcinoma cells produce tubulin-based extensions of the plasma membrane, termed microtentacles (McTNs), which aid in reattachment. CSC and EMT-associated upregulation of intermediate filament vimentin and increased

Invest Ophthalmol Vis Sci. 2014 Mar 20;55(3):1770-9. doi: 10.1167/iovs.13-12988. The Epstein-Barr virus causes epithelial-mesenchymal transition in human corneal epithelial cells via Syk/src and Akt/Erk signaling pathways. Park GB1, Kim D, Kim YS, Kim S, Lee HK, Yang JW, Hur DY. Author information Department of Anatomy and Research Center for Tumor Immunolo...

TY - JOUR. T1 - Activation of ERK1/2-mTORC1-NOX4 mediates TGF-β1-induced epithelial-mesenchymal transition and fibrosis in retinal pigment epithelial cells. AU - Kim, Soo Jin. AU - Kim, Yun Sang. AU - Kim, Jeong Hun. AU - Jang, Ha Young. AU - Ly, Dat Da. AU - Das, Ranjan. AU - Park, Kyu Sang. N1 - Funding Information: This work was supported by the Medical Research Center Program (2017R1A5A2015369) from the Ministry of Science and ICT, and the Korea Health Technology R&D Project through the KHIDI (HI18C2196) from the Ministry of Health & Welfare, and Myung Sun Kim Memorial Foundation (2016). Funding Information: This work was supported by the Medical Research Center Program ( 2017R1A5A2015369 ) from the Ministry of Science and ICT , and the Korea Health Technology R&D Project through the KHIDI ( HI18C2196 ) from the Ministry of Health & Welfare , and Myung Sun Kim Memorial Foundation (2016) . Publisher Copyright: © 2020 Elsevier Inc.. PY - 2020/8/27. Y1 - 2020/8/27. N2 - Transforming growth ...

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Epithelial-mesenchymal transition (EMT) is implicated in the metastatic process and presents a challenge to epithelial cell adhesion molecule-based detection of circulating tumor cells (CTCs), which have been demonstrated to be a prognostic indicator in metastatic breast cancer. Although evidence has indicated that heterogeneity of CTCs based on EMT markers is associated with disease progression, no standard recommendations have been established for clinical practice. This study aimed to evaluate the prognostic significance of dynamic CTC detection based on EMT for metastatic breast cancer patients. We enrolled 108 human epidermal growth factor receptor 2-negative metastatic breast cancer patients from the prospective phase III CAMELLIA study and applied the CanPatrol CTC enrichment technique to identify CTC phenotypes (including epithelial CTCs, biphenotypic epithelial/mesenchymal CTCs, and mesenchymal CTCs) in peripheral blood samples. Receiver operating characteristic curve analyses of total CTC

Previous studies in our laboratory identified that 3-deazaneplanocin A (DZNep), a carbocyclic adenosine analog and histone methyl transferase inhibitor, suppresses TGFβ-induced epithelial-to-mesenchymal (EMT) characteristics. In addition, DZNep epigenetically reprograms miRNAs (miRs) to regulate endogenous TGFbeta1 levels via miR-663/4787 mediated RNA interference (Mol Cancer Res. 2016 Sep 13. pii: molcanres.0083.2016) (1). While DZNep also attenuates exogenous TGFbeta-induced EMT response, the mechanism of this inhibition was unclear. Here, DZNep induced miR-202-5p to target both TGFβ receptors, TGFBR1 and TGFBR2, for RNA interference and thereby contribute to the suppression of exogenous TGFbeta-induced EMT in pancreatic cancer cells. Lentiviral overexpression of miR-202 significantly reduced the protein levels of both TGFbeta receptors and suppressed TGFbeta signaling and EMT phenotypic characteristics of cultured parenchymal pancreatic cancer cells. Consistently, transfection of anti-miRs ...

Breast cancer is one of the most common malignant diseases in women. Epithelial-mesenchymal transition (EMT) has been documented to play an important role in proliferation, invasion and metastasis of tumor cells as well as drug resistance. Even though the signal transducer and activator of transcription 3 (STAT3) is not a master transcription factor of EMT, STAT3 is involved in the regulation of EMT-related gene expression. However, it remains unclear whether targeted inhibitors of STAT3 affect EMT-mediated proliferation, migration, invasion and drug resistance of tumor cells. In this paper, we investigated the effects of STAT3 and its interaction with Twist, a master transcription factor, in EMT program and subsequent changes in proliferation, migration and invasion of breast cancer cells by interfering STAT3 signaling pathway with different strategies such as STAT3 inactivation and STAT3 silencing. Furthermore, we explored the role of inhibiting STAT3 phosphorylation in the EMT regulation of ...

TY - JOUR. T1 - Transcription Factors OVOL1 and OVOL2 Induce the Mesenchymal to Epithelial Transition in Human Cancer. AU - Roca, Hernan. AU - Hernandez, James. AU - Weidner, Savannah. AU - McEachin, Richard C.. AU - Fuller, David. AU - Sud, Sudha. AU - Schumann, Taibriana. AU - Wilkinson, John E.. AU - Zaslavsky, Alexander. AU - Li, Hangwen. AU - Maher, Christopher A.. AU - Daignault-Newton, Stephanie. AU - Healy, Patrick N.. AU - Pienta, Kenneth J.. PY - 2013/10/4. Y1 - 2013/10/4. N2 - Cell plasticity regulated by the balance between the mesenchymal to epithelial transition (MET) and the opposite program, EMT, is critical in the metastatic cascade. Several transcription factors (TFs) are known to regulate EMT, though the mechanisms of MET remain unclear. We demonstrate a novel function of two TFs, OVOL1 and OVOL2, as critical inducers of MET in human cancers. Our findings indicate that the OVOL-TFs control MET through a regulatory feedback loop with EMT-inducing TF ZEB1, and the regulation of ...

The critical role of EGF-beta-catenin signaling in the epithelial-mesenchymal transition in human glioblastoma Xingqiang Wang, Shanshi Wang, Xiaolong Li, Shigang Jin, Feng Xiong, Xin Wang Department of Neurosurgery, Peopleâ s Hospital of Rizhao, Jining Medical University, Rizhao, China Abstract: To date, β-catenin has been reported to be implicated in mediating the epithelial-mesenchymal transition (EMT) in a variety of human cancers, which can be triggered by EGF. However, the mechanisms underlying EGF-β-catenin pathway-induced EMT of glioblastoma multiforme (GBM) have not been reported previously. In the present study, immunohistochemistry, reverse transcription polymerase chain reaction, and Western blot were applied to investigate the effect of EGF-β-catenin pathway on EMT of GBM. Here, we identified that β-catenin mRNA and protein levels were up-regulated in GBM tissues and four kinds of glioblastoma cell lines, including T98G, A172, U87, and U251 cells, compared with normal brain

Fingerprint Dive into the research topics of Epithelial Mesenchymal Transition (EMT) in Metastatic Breast Cancer in Omani Women. Together they form a unique fingerprint. ...

Breast cancer is the leading cause of cancer-associated deaths in women. Lymph node near to the primary breast tumor have a high chance of developing a secondary tumor, representing one of the first signs of metastasis in breast cancer. Metastasis is promoted by epithelial-mesenchymal transition (EMT), process leaded by the transcription factors SNAIL, SLUG, ZEB and TWIST. MicroRNAs are small non-coding RNAs, whose expression has been demonstrated to be altered in different cancer types. Because of their ability to regulate large sets of genes involved in cancer growth and metastasis, microRNAs have emerged as candidate molecular biomarkers and novel therapeutic targets. The aim of this study is to identify microRNAs differentially expressed in breast tumors in relation to EMT-transcription factor expression and lymph node metastasis, and that are involved in epithelial-mesenchymal transition. For this purpose, we used microRNA microarray data from 50 fresh frozen breast tumors with different ...

E-cadherin and its transcriptional repressor Snail1 (Snai1) are two factors that control epithelial phenotype. Expression of Snail1 promotes the conversion of epithelial cells to mesenchymal cells, and occurs concomitantly with the downregulation of E-cadherin and the upregulation of expression of mesenchymal genes such as those encoding fibronectin and LEF1. We studied the molecular mechanism controlling the expression of these genes in mesenchymal cells. Forced expression of E-cadherin strongly downregulated fibronectin and LEF1 RNA levels, indicating that E-cadherin-sensitive factors are involved in the transcription of these genes. E-cadherin overexpression decreased the transcriptional activity of the fibronectin promoter and reduced the interaction of beta-catenin and NF-kappaB with this promoter. Similar to beta-catenin, NF-kappaB was found, by co-immunoprecipitation and pull-down assays, to be associated with E-cadherin and other cell-adhesion components. Interaction of the NF-kappaB p65 ...

During epithelial-mesenchymal transition (EMT) epithelial cancer cells transdifferentiate into highly motile, invasive, mesenchymal-like cells, giving rise to disseminating tumor cells. Few of these disseminated cells successfully metastasize. Immune cells and inflammation in the tumor microenvironment were shown to drive EMT, but few studies investigated the consequences of EMT for tumor immunosurveillance. In addition to initiating metastasis, we demonstrate that EMT confers increased susceptibility to natural killer (NK) cells and contributes, in part, to the inefficiency of the metastatic process. Depletion of NK cells allowed spontaneous metastasis without affecting primary tumor growth. EMT-induced modulation of E-cadherin and cell adhesion molecule 1 (CADM1) mediated increased susceptibility to NK cytotoxicity. Higher CADM1 expression correlates with improved patient survival in 2 lung and 1 breast adenocarcinoma patient cohorts and decreased metastasis. Our observations reveal a novel ...

During epithelial-mesenchymal transition (EMT) epithelial cancer cells trans-differentiate into highly-motile, invasive, mesenchymal-like cells giving rise to disseminating tumor cells. Only few of these disseminated cells successfully metastasize. Immune cells and inflammation in the tumor microenvironment was shown to drive EMT, but few studies investigated the consequences of EMT on tumor immunosurveillance. In addition to initiating metastasis, we demonstrate that EMT confers increased susceptibility to NK cells and contributes, in part, to the inefficiency of the metastatic process. Depletion of NK cells allowed spontaneous metastasis without effecting primary tumor growth. EMT-induced modulation of E-cadherin and cell adhesion molecule 1 (CADM1) mediated increased susceptibility to NK cytotoxicity. Higher CADM1 expression correlates with improved patient survival in two lung and one breast adenocarcinoma patient cohorts and decreased metastasis. Our observation reveal a novel NK-mediated, ...

During epithelial-mesenchymal transition (EMT) epithelial cancer cells trans-differentiate into highly-motile, invasive, mesenchymal-like cells giving rise to disseminating tumor cells. Only few of these disseminated cells successfully metastasize. Immune cells and inflammation in the tumor microenvironment was shown to drive EMT, but few studies investigated the consequences of EMT on tumor immunosurveillance. In addition to initiating metastasis, we demonstrate that EMT confers increased susceptibility to NK cells and contributes, in part, to the inefficiency of the metastatic process. Depletion of NK cells allowed spontaneous metastasis without effecting primary tumor growth. EMT-induced modulation of E-cadherin and cell adhesion molecule 1 (CADM1) mediated increased susceptibility to NK cytotoxicity. Higher CADM1 expression correlates with improved patient survival in two lung and one breast adenocarcinoma patient cohorts and decreased metastasis. Our observation reveal a novel NK-mediated, ...

During epithelial-mesenchymal transition (EMT) epithelial cancer cells trans-differentiate into highly-motile, invasive, mesenchymal-like cells giving rise to disseminating tumor cells. Only few of these disseminated cells successfully metastasize. Immune cells and inflammation in the tumor microenvironment was shown to drive EMT, but few studies investigated the consequences of EMT on tumor immunosurveillance. In addition to initiating metastasis, we demonstrate that EMT confers increased susceptibility to NK cells and contributes, in part, to the inefficiency of the metastatic process. Depletion of NK cells allowed spontaneous metastasis without effecting primary tumor growth. EMT-induced modulation of E-cadherin and cell adhesion molecule 1 (CADM1) mediated increased susceptibility to NK cytotoxicity. Higher CADM1 expression correlates with improved patient survival in two lung and one breast adenocarcinoma patient cohorts and decreased metastasis. Our observation reveal a novel NK-mediated, ...

During epithelial-mesenchymal transition (EMT) epithelial cancer cells trans-differentiate into highly-motile, invasive, mesenchymal-like cells giving rise to disseminating tumor cells. Only few of these disseminated cells successfully metastasize. Immune cells and inflammation in the tumor microenvironment was shown to drive EMT, but few studies investigated the consequences of EMT on tumor immunosurveillance. In addition to initiating metastasis, we demonstrate that EMT confers increased susceptibility to NK cells and contributes, in part, to the inefficiency of the metastatic process. Depletion of NK cells allowed spontaneous metastasis without effecting primary tumor growth. EMT-induced modulation of E-cadherin and cell adhesion molecule 1 (CADM1) mediated increased susceptibility to NK cytotoxicity. Higher CADM1 expression correlates with improved patient survival in two lung and one breast adenocarcinoma patient cohorts and decreased metastasis. Our observation reveal a novel NK-mediated, ...

During epithelial-mesenchymal transition (EMT) epithelial cancer cells trans-differentiate into highly-motile, invasive, mesenchymal-like cells giving rise to disseminating tumor cells. Only few of these disseminated cells successfully metastasize. Immune cells and inflammation in the tumor microenvironment was shown to drive EMT, but few studies investigated the consequences of EMT on tumor immunosurveillance. In addition to initiating metastasis, we demonstrate that EMT confers increased susceptibility to NK cells and contributes, in part, to the inefficiency of the metastatic process. Depletion of NK cells allowed spontaneous metastasis without effecting primary tumor growth. EMT-induced modulation of E-cadherin and cell adhesion molecule 1 (CADM1) mediated increased susceptibility to NK cytotoxicity. Higher CADM1 expression correlates with improved patient survival in two lung and one breast adenocarcinoma patient cohorts and decreased metastasis. Our observation reveal a novel NK-mediated, ...

During epithelial-mesenchymal transition (EMT) epithelial cancer cells trans-differentiate into highly-motile, invasive, mesenchymal-like cells giving rise to disseminating tumor cells. Only few of these disseminated cells successfully metastasize. Immune cells and inflammation in the tumor microenvironment was shown to drive EMT, but few studies investigated the consequences of EMT on tumor immunosurveillance. In addition to initiating metastasis, we demonstrate that EMT confers increased susceptibility to NK cells and contributes, in part, to the inefficiency of the metastatic process. Depletion of NK cells allowed spontaneous metastasis without effecting primary tumor growth. EMT-induced modulation of E-cadherin and cell adhesion molecule 1 (CADM1) mediated increased susceptibility to NK cytotoxicity. Higher CADM1 expression correlates with improved patient survival in two lung and one breast adenocarcinoma patient cohorts and decreased metastasis. Our observation reveal a novel NK-mediated, ...

During epithelial-mesenchymal transition (EMT) epithelial cancer cells trans-differentiate into highly-motile, invasive, mesenchymal-like cells giving rise to disseminating tumor cells. Only few of these disseminated cells successfully metastasize. Immune cells and inflammation in the tumor microenvironment was shown to drive EMT, but few studies investigated the consequences of EMT on tumor immunosurveillance. In addition to initiating metastasis, we demonstrate that EMT confers increased susceptibility to NK cells and contributes, in part, to the inefficiency of the metastatic process. Depletion of NK cells allowed spontaneous metastasis without effecting primary tumor growth. EMT-induced modulation of E-cadherin and cell adhesion molecule 1 (CADM1) mediated increased susceptibility to NK cytotoxicity. Higher CADM1 expression correlates with improved patient survival in two lung and one breast adenocarcinoma patient cohorts and decreased metastasis. Our observation reveal a novel NK-mediated, ...

During epithelial-mesenchymal transition (EMT) epithelial cancer cells trans-differentiate into highly-motile, invasive, mesenchymal-like cells giving rise to disseminating tumor cells. Only few of these disseminated cells successfully metastasize. Immune cells and inflammation in the tumor microenvironment was shown to drive EMT, but few studies investigated the consequences of EMT on tumor immunosurveillance. In addition to initiating metastasis, we demonstrate that EMT confers increased susceptibility to NK cells and contributes, in part, to the inefficiency of the metastatic process. Depletion of NK cells allowed spontaneous metastasis without effecting primary tumor growth. EMT-induced modulation of E-cadherin and cell adhesion molecule 1 (CADM1) mediated increased susceptibility to NK cytotoxicity. Higher CADM1 expression correlates with improved patient survival in two lung and one breast adenocarcinoma patient cohorts and decreased metastasis. Our observation reveal a novel NK-mediated, ...

Increasing evidence points to the role of EMT in cancer progression, metastasis and drug resistance. However, the difficulty in making an adequate assessment of EMT in tumours has caused dispute as to whether EMT exists in cancer (Jordan et al, 2011). To address this issue, we developed a generic EMT signature to quantitatively estimate the extent of EMT in tumours and cell lines. To the best of our knowledge, this is the first time a generic EMT signature has been sought in order to capture the universal features of EMT in tumours or in cells. Previous reports indicate that intermediate states of EMT display the highest plasticity (Jordan et al, 2011; Huang et al, 2013) and thus represent an appropriate stage within which to induce or reverse EMT. The change in EMT score captures and reflects this phenotypic transition in the cell or tissue; this method is judiciously illustrated in a previous application where Epi MCF7 breast cancer cells displayed a shift in the EMT spectrum when transfected ...

Although the model proposed in Fig. 7 captures the effects observed in the two cell lines explored here in most detail (H322 and HPAF-II), it should be emphasized that not all aspects of the model held in other cell lines. For example, although SHP2 knockdown clearly increased baseline epithelial characteristics in H358 and CAPAN-2 cells (and indeed most of the cell lines analyzed in Fig. 3), EGF did not substantially augment EMT in response to TGFβ in those cell lines. At least within the panel of cell lines we tested, this might suggest a broader relevance of basal SHP2 activity than growth factor-induced SHP2 activity in determining epithelial or mesenchymal characteristics. The results in Fig. S4 offer one possible explanation for the inability of EGF to augment TGFβ-mediated EMT in some cell lines.. Based on our previous work and evidence from other studies demonstrating the importance of ERK activity in EMT (Shin et al., 2010; Buonato and Lazzara, 2014), SHP2-mediated augmentation of ERK ...

Initiation of metastasis requires invasion, which is enabled by EMT.[36][37] Carcinoma cells in a primary tumor lose cell-cell adhesion mediated by E-cadherin repression and break through the basement membrane with increased invasive properties, and enter the bloodstream through intravasation. Later, when these circulating tumor cells (CTCs) exit the bloodstream to form micro-metastases, they undergo MET for clonal outgrowth at these metastatic sites. Thus, EMT and MET form the initiation and completion of the invasion-metastasis cascade.[38] At this new metastatic site, the tumor may undergo other processes to optimize growth. For example, EMT has been associated with PD-L1 expression, particularly in lung cancer. Increased levels of PD-L1 suppresses the immune system which allows the cancer to spread more easily. [39] EMT confers resistance to oncogene-induced premature senescence. Twist1 and Twist2, as well as ZEB1 protects human cells and mouse embryonic fibroblasts from senescence. ...

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The ability of cancer to adapt renders it one of the most challenging pathologies of all time. It is the most dreaded pathological entity because of its capacity to metastasize to distant sites in the body, and 90% of all cancer-related deaths recorded to date are attributed to metastasis. Currently, three main theories have been proposed to explain the metastatic pathway of cancer: the epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) hypothesis (1), the cancer stem cell hypothesis (2), and the macrophage-cancer cell fusion hybrid hypothesis (3). We propose a new hypothesis, i.e., under the effect of particular biochemical and/or physical stressors, cancer cells can undergo nuclear expulsion with subsequent macrophage engulfment and fusion, with the formation of cancer fusion cells (CFCs). The existence of CFCs, if confirmed, would represent a novel metastatic pathway and a shift in the extant dogma of cancer; consequently, new treatment targets would be ...

Introduction: One of the possible sources of myofibroblasts accumulation in IPF is the trans-differentiation of the injured alveolar epithelial cells to myofibroblasts through EMT process. Studies so far suggest that TGFβ1 and EGFR signalling cascades are activated during lung fibrosis. We hypothesized that TGFb1 signalling requires EGFR activation to induce EMT during lung fibrosis.. Material and methods: To address the role of EGFR cascades in TGFβ1-induced EMT, immortalized human bronchial epithelial cells (iHBECs) were treated with or without TGFβ1 (2ng/ml), different concentrations of EGF and EGFR tyrosine kinase inhibitor (AG1478) for 3 days. Expression of the epithelial marker E-cadherin and the mesenchymal marker α-smooth muscle actin (αSMA) was examined by flow cytometry, Western blot and, immunocytochemistry staining. EGFR and Smad2 phosphorylation was measured by Western blot.. Results: Stimulation of iHBECs with TGFβ1 down-regulated E-cadherin expression and increased α-SMA ...