Troglitazone ameliorates high glucose-induced EMT and dysfunction of SGLTs through PI3K/Akt, GSK-3beta, Snail1, and beta-catenin in renal proximal tubule cells.
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Multidrug resistance in breast cancer cells during epithelial-mesenchymal transition is modulated by breast cancer resistant protein.
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BACKGROUND AND OBJECTIVE: Epithelial-mesenchymal transition (EMT) not only initiates invasion and metastasis of tumors, but also induces multidrug resistance in tumor cells. Our experiment analyzed the dependability between breast cancer resistant protein (BCRP) and EMT in breast cancer to explore the effect of EMT on BCRP-mediated multidrug resistance. METHODS: The expressions of BCRP and transcription inhibitor Snai1 (Snail) in breast cancer were detected by immunohistochemistry. The eukaryotic expression vector pCDNA3.1-Snail was constructed and then transfected into human breast cancer cell line MCF-7. Snail, epithelial marker gene E-cadherin, interstitial marker gene Vimentin, multidrug resistance protein BCRP, and relative drug resistance were measured by immunofluorescence, Western blot, real-time polymerase chain reaction (PCR), and MTT assay. RESULTS: Immunohistochemistry showed that Snail was highly correlated with BCRP in breast cancer. Immunofluorescence, Western blot, real-time PCR revealed that compared with parent cell MCF-7, after transfected with Snail, the expression of E-cadherin in MCF-7 decreased, but Snail, Vimentin, and BCRP increased. MTT displayed that the relative drug resistance increased to 9.93. CONCLUSION: After transfected with eukaryotic expression vector pCDNA3.1-Snail, breast cancer cells MCF-7 showed EMT with BCRP-mediated multidrug resistance. (+info)
Epithelial-myoepithelial carcinoma of the tongue base: a case for the case-report and review of the literature.
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Transitions between epithelial and mesenchymal states and the morphogenesis of the early mouse embryo.
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Multicellular organisms arise from the generation of different cell types and the organization of cells into tissues and organs. Cells of metazoa display two main phenotypes, the ancestral epithelial state and the recent mesenchymal derivative. Epithelial cells are usually stationary and reside in two-dimensional sheets. By contrast mesenchymal cells are loosely packed and can move to new positions, thereby providing a vehicle for cell rearrangement, dispersal and novel cell-cell interactions. Transitions between epithelial and mesenchymal states drive key morphogenetic events in the early vertebrate embryo, including gastrulation, germ layer formation and somitogenesis. The cell behaviors and molecular mechanisms promoting transitions between these two states in the early mouse embryo are discussed in this review. (+info)
Epithelial to mesenchymal transition in human skin wound healing is induced by tumor necrosis factor-alpha through bone morphogenic protein-2.
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Role of beta5-integrin in epithelial-mesenchymal transition in response to TGF-beta.
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Epithelial-mesenchymal-transition (EMT) in response to TGFbeta contributes to normal development, wound healing and tumor progression. The present study provides evidence for a critical role of beta5-integrin in the TGFbeta-induced EMT and the tumorigenic potential of carcinoma cells. We show that the alphavbeta-integrin subunits are upregulated during the TGFbeta-induced EMT and this response requires Smad transcription factors. Depletion of alphav-integrin by siRNA blocked the EMT response whereas knock-down of beta1-integrin had no effect. Importantly, depletion of beta5-integrin blocked the TGFbeta-induced EMT impairing adhesion to cell-matrix and integrin signaling, but did not change expression of E-cadherin and TGFbeta-target genes. Accordingly, the EMT process and integrin signaling were blocked by cRGD peptide interfering with cell-matrix adhesion or by inhibition of focal adhesion kinase, indicating the importance of beta5-integrin-mediated adhesions in EMT. Finally, depletion of beta5-integrin significantly reduced invasiveness of breast carcinoma cells. Thus, the beta5-integrin adhesions contribute to the TGFbeta-induced EMT and the tumorigenic potential of carcinoma cells. (+info)
The cessation of gastrulation: BMP signaling and EMT during and at the end of gastrulation.
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An integral component of gastrulation in all organisms is epithelial to mesenchymal transition (EMT), a fundamental morphogenetic event through which epithelial cells transform into mesenchymal cells. The mesenchymal cells that arise from epithelial cells during gastrulation contribute to various tissue rudiments during subsequent development, including the notochord, somites, heart, gut, kidney, body wall and lining of the coelom. The process of gastrulation has been the subject of several hundred scientific papers. Despite all that has been written, it is likely that what we currently know about gastrulation is still considerably less than what remains to be learned. One critical remaining question that we consider here is how does gastrulation cease at the right place along the body axis, and at the right time? In this commentary, we focus on the molecular mechanism for the cessation of gastrulation, using the chick embryo as a model system. (+info)
Epithelial to mesenchymal transition in gingival overgrowth.
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