Hep G2 Cells
Carcinoma, Hepatocellular
Tumor Cells, Cultured
Emetics
Plasminogen Inactivators
Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent
Lovastatin
Liver
Apolipoprotein A-I
Artificial Organs
Asialoglycoprotein Receptor
Carboxypeptidase H
Receptors, LDL
Hepatoblastoma
RNA, Messenger
Oxaloacetic Acid
Moraceae
Lipoproteins, LDL
Apolipoproteins A
Oleic Acid
Apolipoproteins B
Hydroxymethylglutaryl CoA Reductases
Cholesterol
Immunosorbent Techniques
Primaquine
Lipoproteins, HDL
Oleic Acids
Asialoglycoproteins
Cycloheximide
Immunoelectrophoresis, Two-Dimensional
Tunicamycin
Apolipoprotein A-II
Blotting, Northern
Transfection
Albumins
Chenodeoxycholic Acid
Transcription, Genetic
Vitamin K
Cytochrome P-450 CYP2E1
Apolipoprotein B-100
Base Sequence
Sterol O-Acyltransferase
Biological Transport
Molecular Sequence Data
Gene Expression Regulation
Glycoproteins
Promoter Regions, Genetic
Electrophoresis, Polyacrylamide Gel
Carboxypeptidases
Lipoproteins
Prealbumin
Cholesterol Esters
Bile Acids and Salts
Chloramphenicol O-Acetyltransferase
DNA
Antineoplastic Agents, Phytogenic
Carboxylic Ester Hydrolases
Chromatography, Affinity
Fibrinogen
L-Lactate Dehydrogenase
Protein Synthesis Inhibitors
Endocytosis
Apolipoproteins
Lipoproteins, VLDL
Iodine Radioisotopes
Culture Media
Carrier Proteins
Antioxidants
Receptors, Cell Surface
Plasmids
Cells, Cultured
Glutathione
Dose-Response Relationship, Drug
Blotting, Western
Glycosylation
Cloning, Molecular
Cytochrome P-450 Enzyme System
Amino Acid Sequence
Protein Processing, Post-Translational
Apolipoproteins E
Cell Survival
Ascorbic Acid
Insulin
Protein Biosynthesis
Cell Division
Tetradecanoylphorbol Acetate
Lipid Peroxidation
Glucose
Binding, Competitive
Mitochondria
Cell Membrane
Apoptosis
Gene Expression
Binding Sites
Gene Amplification
Cell Nucleus
DNA-Binding Proteins
Microscopy, Electron
Transcription Factors
Reactive Oxygen Species
Polymerase Chain Reaction
Apoptosis of human hepatoma cell lines induced by transforming growth factor beta 1 (TGF-beta1) correlates with p53 and Smad4 activation. (1/2073)
OBJECTIVE: To determine the relationships between apoptosis induced by transforming growth factor beta 1(TGF-beta1) and Smad in human hepatoma cell lines. METHODS: Three human hepatic carcinoma cell lines, involving different status of the p53 gene respectively, were used in this study. TGF-beta1-induced apoptosis in hepatic carcinoma cell lines was quantitated using the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. For identification of the mechanism of apoptosis induced by TGF-beta1, these cell lines were transfected with a TGF-beta1-inducible luciferase reporter plasmid containing Smad binding elements (SBE) and luciferase gene using LF2000, then were treated with TGF-beta1. Relative luciferase activity was assayed respectively. RESULTS: Among three cell lines studied with TUNEL assay, addition of TGF-beta1 induced apoptosis only in HepG2 cells (wild type p53). In contrast, Huh-7 (mutant p53) and Hep3B (deleted p53) cell lines lacked apoptosis. The detection of luciferase activity indicated that HepG2 cells dramatically increased the response to TGF-beta1 induction, Huh-7 and Hep3B cell lines significantly lowered luciferase expression. CONCLUSION: HepG2 cells were highly susceptible to TGF-beta1-induced apoptosis compared with Hep3B and Huh-7 cell lines. Smad4 may be a central mediator of the TGF-beta1 signaling transduction pathway. (+info)Effect of the venom of the spider Macrothele raveni on the expression of p21 gene in HepG2 cells. (2/2073)
This paper focuses on the effect of the venom of the spider Macrothele raveni on the proliferation of human hepatocelluar carcinoma cell line HepG2 and the related molecular mechanism. XTT test showed that the proliferation of HepG2 cells in vitro was inhibited by the spider venom (P<0.05) in a concentration-dependent manner. By using flow cytometry, it was found that the spider venom caused selective G(2)/M cell cycle arrest in HepG2 cells. RT-PCR and Western blot indicated the expressions of p21 mRNA and protein in HepG2 cells were obviously up-regulated by the spider venom. The venom of the spider Macrothele raveni inhibited the proliferation of HepG2 cells. These results suggest that the possible mechanism of the spider venom is to activate the expressions of p21 gene and protein and to cause selective cell cycle arrest at G(2)/M phase, leading to HepG2 cell apoptosis. (+info)Host gene expression profiling of dengue virus infection in cell lines and patients. (3/2073)
BACKGROUND: Despite the seriousness of dengue-related disease, with an estimated 50-100 million cases of dengue fever and 250,000-500,000 cases of dengue hemorrhagic fever/dengue shock syndrome each year, a clear understanding of dengue pathogenesis remains elusive. Because of the lack of a disease model in animals and the complex immune interaction in dengue infection, the study of host response and immunopathogenesis is difficult. The development of genomics technology, microarray and high throughput quantitative PCR have allowed researchers to study gene expression changes on a much broader scale. We therefore used this approach to investigate the host response in dengue virus-infected cell lines and in patients developing dengue fever. METHODOLOGY/PRINCIPAL FINDINGS: Using microarray and high throughput quantitative PCR method to monitor the host response to dengue viral replication in cell line infection models and in dengue patient blood samples, we identified differentially expressed genes along three major pathways; NF-kappaB initiated immune responses, type I interferon (IFN) and the ubiquitin proteasome pathway. Among the most highly upregulated genes were the chemokines IP-10 and I-TAC, both ligands of the CXCR3 receptor. Increased expression of IP-10 and I-TAC in the peripheral blood of ten patients at the early onset of fever was confirmed by ELISA. A highly upregulated gene in the IFN pathway, viperin, was overexpressed in A549 cells resulting in a significant reduction in viral replication. The upregulation of genes in the ubiquitin-proteasome pathway prompted the testing of proteasome inhibitors MG-132 and ALLN, both of which reduced viral replication. CONCLUSION/SIGNIFICANCE: Unbiased gene expression analysis has identified new host genes associated with dengue infection, which we have validated in functional studies. We showed that some parts of the host response can be used as potential biomarkers for the disease while others can be used to control dengue viral replication, thus representing viable targets for drug therapy. (+info)Structural antitumoral activity relationships of synthetic chalcones. (4/2073)
(+info)Malathion-induced oxidative stress, cytotoxicity, and genotoxicity in human liver carcinoma (HepG2) cells. (5/2073)
(+info)The antitumoral effect of Paris Saponin I associated with the induction of apoptosis through the mitochondrial pathway. (6/2073)
(+info)Activation of PXR induces hypercholesterolemia in wild-type and accelerates atherosclerosis in apoE deficient mice. (7/2073)
(+info)Vitamin K2 suppresses proliferation and motility of hepatocellular carcinoma cells by activating steroid and xenobiotic receptor. (8/2073)
Vitamin K2, known as a cofactor for gamma-carboxylase, also serves as a ligand of a nuclear receptor, Steroid and Xenobiotic Receptor (SXR). Several clinical trials revealed that vitamin K2 reduced de novo formation and recurrence of hepatocellular carcinoma (HCC). To examine the role of SXR in HCC as a receptor activated by vitamin K2, the cells stably overexpressing SXR were established using a HCC cell line, HuH7. Overexpression of SXR resulted in reduced proliferation and motility of the cells. Further suppression of proliferation and motility was observed when SXR overexpressing clones were treated with vitamin K2. These results suggest that the activation of SXR could contribute to tumor suppressive effects of vitamin K2 on HCC cells. (+info)There are several risk factors for developing HCC, including:
* Cirrhosis, which can be caused by heavy alcohol consumption, viral hepatitis (such as hepatitis B and C), or fatty liver disease
* Family history of liver disease
* Chronic obstructive pulmonary disease (COPD)
* Diabetes
* Obesity
HCC can be challenging to diagnose, as the symptoms are non-specific and can be similar to those of other conditions. However, some common symptoms of HCC include:
* Yellowing of the skin and eyes (jaundice)
* Fatigue
* Loss of appetite
* Abdominal pain or discomfort
* Weight loss
If HCC is suspected, a doctor may perform several tests to confirm the diagnosis, including:
* Imaging tests, such as ultrasound, CT scan, or MRI, to look for tumors in the liver
* Blood tests to check for liver function and detect certain substances that are produced by the liver
* Biopsy, which involves removing a small sample of tissue from the liver to examine under a microscope
Once HCC is diagnosed, treatment options will depend on several factors, including the stage and location of the cancer, the patient's overall health, and their personal preferences. Treatment options may include:
* Surgery to remove the tumor or parts of the liver
* Ablation, which involves destroying the cancer cells using heat or cold
* Chemoembolization, which involves injecting chemotherapy drugs into the hepatic artery to reach the cancer cells
* Targeted therapy, which uses drugs or other substances to target specific molecules that are involved in the growth and spread of the cancer
Overall, the prognosis for HCC is poor, with a 5-year survival rate of approximately 20%. However, early detection and treatment can improve outcomes. It is important for individuals at high risk for HCC to be monitored regularly by a healthcare provider, and to seek medical attention if they experience any symptoms.
Liver neoplasms, also known as liver tumors or hepatic tumors, are abnormal growths of tissue in the liver. These growths can be benign (non-cancerous) or malignant (cancerous). Malignant liver tumors can be primary, meaning they originate in the liver, or metastatic, meaning they spread to the liver from another part of the body.
There are several types of liver neoplasms, including:
1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and arises from the main cells of the liver (hepatocytes). HCC is often associated with cirrhosis and can be caused by viral hepatitis or alcohol abuse.
2. Cholangiocarcinoma: This type of cancer arises from the cells lining the bile ducts within the liver (cholangiocytes). Cholangiocarcinoma is rare and often diagnosed at an advanced stage.
3. Hemangiosarcoma: This is a rare type of cancer that originates in the blood vessels of the liver. It is most commonly seen in dogs but can also occur in humans.
4. Fibromas: These are benign tumors that arise from the connective tissue of the liver (fibrocytes). Fibromas are usually small and do not spread to other parts of the body.
5. Adenomas: These are benign tumors that arise from the glandular cells of the liver (hepatocytes). Adenomas are usually small and do not spread to other parts of the body.
The symptoms of liver neoplasms vary depending on their size, location, and whether they are benign or malignant. Common symptoms include abdominal pain, fatigue, weight loss, and jaundice (yellowing of the skin and eyes). Diagnosis is typically made through a combination of imaging tests such as CT scans, MRI scans, and ultrasound, and a biopsy to confirm the presence of cancer cells.
Treatment options for liver neoplasms depend on the type, size, location, and stage of the tumor, as well as the patient's overall health. Surgery may be an option for some patients with small, localized tumors, while others may require chemotherapy or radiation therapy to shrink the tumor before surgery can be performed. In some cases, liver transplantation may be necessary.
Prognosis for liver neoplasms varies depending on the type and stage of the cancer. In general, early detection and treatment improve the prognosis, while advanced-stage disease is associated with a poorer prognosis.
The exact cause of hepatoblastoma is not known, but it is believed to be linked to genetic mutations that occur during fetal development. Children with certain congenital conditions, such as Beckwith-Wiedemann syndrome, are at higher risk of developing hepatoblastoma. The symptoms of hepatoblastoma can include abdominal pain, weight loss, and jaundice (yellowing of the skin and eyes), but in many cases, the cancer may not cause any noticeable symptoms until it has reached an advanced stage.
Hepatoblastoma is diagnosed through a combination of imaging tests, such as ultrasound, CT scans, and MRI, and a biopsy to confirm the presence of cancer cells. Treatment typically involves surgery to remove the affected lobe of the liver, followed by chemotherapy to kill any remaining cancer cells. In some cases, a liver transplant may be necessary if the cancer has spread too far or if the child's liver is not functioning properly. The prognosis for hepatoblastoma depends on several factors, including the stage of the cancer at diagnosis and the effectiveness of treatment. With current treatments, the 5-year survival rate for children with hepatoblastoma is around 70%.
Examples of experimental liver neoplasms include:
1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and can be induced experimentally by injecting carcinogens such as diethylnitrosamine (DEN) or dimethylbenz(a)anthracene (DMBA) into the liver tissue of animals.
2. Cholangiocarcinoma: This type of cancer originates in the bile ducts within the liver and can be induced experimentally by injecting chemical carcinogens such as DEN or DMBA into the bile ducts of animals.
3. Hepatoblastoma: This is a rare type of liver cancer that primarily affects children and can be induced experimentally by administering chemotherapy drugs to newborn mice or rats.
4. Metastatic tumors: These are tumors that originate in other parts of the body and spread to the liver through the bloodstream or lymphatic system. Experimental models of metastatic tumors can be studied by injecting cancer cells into the liver tissue of animals.
The study of experimental liver neoplasms is important for understanding the underlying mechanisms of liver cancer development and progression, as well as identifying potential therapeutic targets for the treatment of this disease. Animal models can be used to test the efficacy of new drugs or therapies before they are tested in humans, which can help to accelerate the development of new treatments for liver cancer.
Interleukin 19
Lipoprotein(a)
IGFBP1
Gamma-glutamyltransferase 1
Hep G2
Wei-Shou Hu
Ecklonia stolonifera
Bakuchiol
Bruce Roth
FGF21
Parathyroid hormone-related protein
Xylaria hypoxylon
ING4
Bufotalin
Cantharidin
Dicycloplatin
Apolipoprotein A-II
GADD45G
Solute carrier organic anion transporter family member 1A2
Pearsonothuria
Calotropis gigantea
Mustakone
Liver sinusoidal endothelial cell
Anticancer gene
Aspergillus flavus
Fermilab
Sickle cell nephropathy
Aflatoxin B1
List of unsolved problems in physics
Francis Farley
NEDD9
Large numbers
Genetic history of the African diaspora
Foodborne illness
Apoptosis
List of atheists (miscellaneous)
CCL5
Human betaherpesvirus 7
Antinuclear antibody
Sun
Bladder cancer
The anticancer effects of thymol on HepG2 cell line. | Med Oncol;40(9): 260, 2023 Aug 05. | MEDLINE
Therapeutic Properties of Stingless Bee Honey in Comparison with European Bee Honey
Microglia LPS-Related Module Antibody Sampler Kit | Cell Signaling Technology
Recombinant Anti-Amyloid Precursor Protein antibody [EPR5118-34] KO Tested (ab126732)
DeCS
DeCS 2010 - Novos termos
NHANES III Laboratory Data File
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ICTRP Search Portal
The Science of Gene-Environment Interaction at the Centers for Disease Control and Prevention and Agency for Toxic Substances...
CDC - Chronic Kidney Disease - Glossary
CDC Science Clips
Inhibitory effect of interleukin-1alpha-induced apoptosis by Polygala tenuifolia in Hep G2 cells - PubMed
Table - SARS-associated Coronavirus Replication in Cell Lines - Volume 12, Number 1-January 2006 - Emerging Infectious Diseases...
Publication Detail
Biomarkers Search
Cascara Sagrada: MedlinePlus Supplements
Lack of Effect of Lamivudine on Ebola Virus Replication - Volume 21, Number 3-March 2015 - Emerging Infectious Diseases journal...
DeCS 2010 - Novos termos
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DeCS 2010 - New terms
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DeCS 2010 - Novos termos
Keywords
Line10
- The anticancer effects of thymol on HepG2 cell line. (bvsalud.org)
- The present study was designed to evaluate possible cytotoxic, genotoxic, apoptotic, oxidant and antioxidant effects of thymol on hepatocellular carcinoma (HepG2) cell line . (bvsalud.org)
- The cytotoxic effect of thymol on HepG2 cell line was determined by XTT test. (bvsalud.org)
- We also used the HUVEC cell line to show whether thymol damages healthy cells . (bvsalud.org)
- The thymol IC50 dose was found to be 11 µM on HepG2 cell line. (bvsalud.org)
- This dose had no lethal effect on the healthy HUVEC cell line. (bvsalud.org)
- Our results suggest that thymol decreases oxidative stress in HepG2 cell line, but it induces apoptosis and genotoxicity . (bvsalud.org)
- Using the human hepatoma cell line Hep G2, we have studied a possible role of protein kinase C (PKC) activity for regulation of erythropoietin (EPO) production. (ox.ac.uk)
- Flow cytometric analysis of Raw 264.7 cells using IKKε (D61F9) XP ® Rabbit mAb (solid line) compared to concentration-matched Rabbit (DA1E) mAb IgG XP ® Isotype Control #3900 (dashed line). (cellsignal.com)
- A human liver tumor cell line used to study a variety of liver-specific metabolic functions. (nih.gov)
Flow3
- Apoptosis of cells was detected in flow cytometry with Annexin V apoptosis kit. (bvsalud.org)
- Flow cytometric analysis of Daudi cells (blue) and MJ cells (green) using Lamin A/C (4C11) Mouse mAb (solid lines) or concentration-matched Mouse (G3A1) mAb IgG1 Isotype Control #5415 (dashed lines). (cellsignal.com)
- Flow cytometric analysis of fixed and permeabilized Jurkat cells using Integrin α4 (D2E1) XP ® Rabbit mAb (blue) compared to concentration-matched Rabbit (DA1E) mAb IgG XP ® Isotype Control #3900 (red). (cellsignal.com)
Control3
- While thymol significantly decreased the TOS level, it increased the TAS level significantly in HepG2 cells compared to control. (bvsalud.org)
- Western blot analysis of extracts from control HeLa cells (lane 1) or HeLa cells with an apparent in-frame truncation mutation in the gene encoding LMNA (lane 2) using Lamin A/C (4C11) Mouse mAb #4777 (upper) or α-actinin (D6F6) XP ® Rabbit mAb #6487 (lower). (cellsignal.com)
- Immunoprecipitation of Rab11FIP1 from HeLa cell extracts using Rabbit (DA1E) mAb IgG XP ® Isotype Control #3900 (lane 2) or Rab11FIP1 (D9D8P) Rabbit mAb (lane 3). (cellsignal.com)
Effect1
- A 24-h preincubation of the cells with PMA (100 nM) virtually blunted the effect of hypoxia on EPO formation. (ox.ac.uk)
Kidney1
- Three cell lines were tested: Vero E6 (African green monkey kidney, ATCC CRL-1586), Hep G2 (human hepatoma, ATCC HB-8065), and human monocyte-derived macrophages. (cdc.gov)
Gene4
- 3. Adenovirus-mediated expression of spermidine/spermine N1-acetyltransferase gene induces S-phase arrest in human colorectal cancer cells. (nih.gov)
- 7. [Construction of recombinant adenovirus vector of hNRAGE gene and its effect on cell cycle of 293 cells]. (nih.gov)
- 9. Two active copies of the X-linked gene spermidine/spermine N1-acetyltransferase (SSAT) in a female lung cancer cell line are associated with an increase in sensitivity to an antitumor polyamine analogue. (nih.gov)
- 12. Expression of a recombinant vector of a mutant human telomerase reverse transcriptase gene in human bladder cancer cell line T24, and its clinical significance. (nih.gov)
Human4
- A human hepatoma cell line, Hep G2 cells are reliable for the study of alcohol-induced hepatotoxicity. (nih.gov)
- 5. Spermidine/spermine N1-acetyltransferase transient overexpression restores sensitivity of resistant human ovarian cancer cells to N1,N12-bis(ethyl)spermine and to cisplatin. (nih.gov)
- A human liver tumor cell line used to study a variety of liver-specific metabolic functions. (bvsalud.org)
- Therefore, we also assessed HepG2 cells and primary human monocyte-derived macrophages sensitive to EBOV infection. (cdc.gov)
Infection4
- The activity of lamivudine against EBOV infection was evaluated in a cell-based ELISA with 1995 isolate EBOV H. sapiens -tc/COD/1995/Kikwit (EBOV/Kik) ( 3 ). (cdc.gov)
- Sigma-Aldrich, St. Louis, MO, USA) was used as a positive control for activity against EBOV and tested at 2-fold dilutions starting at 25 µmol/L. One hour after drug addition, the cells were infected at a multiplicity of infection of 0.5 or 1 with EBOV/Kik. (cdc.gov)
- At 48 hours after infection, cells were formalin-fixed and stained with a primary antibody against EBOV (antibodies against viral matrix protein or glycoprotein) and a secondary antibody (Alexa-488 or horseradish peroxidase). (cdc.gov)
- Chronic hepatitis B infection, caused by the hepatitis B virus (HBV) and exposure to aflatoxins is fundamental in the formation of HCC in developing countries. (who.int)
Clinical1
- 3. Subject has an APOL1 genotype of G1/G1, G2/G2, or G1/G2 obtained with a Vertex designated investigational clinical study assay. (who.int)
Virus6
- Entry of tiger frog virus (an Iridovirus) into HepG2 cells via a pH-dependent, atypical, caveola-mediated endocytosis pathway. (bvsalud.org)
- This atypical caveola -mediated endocytosis is different from the clathrin -mediated endocytosis of frog virus 3 (FV3) by BHK cells , which has been recognized as a model for iridoviruses . (bvsalud.org)
- 16. [Inhibitory effects of ODC and AdoMetDC bi-antisense virus on the growth and invasion of lung cancer cell A-549]. (nih.gov)
- Lamivudine is a nucleoside analog reverse transcription inhibitor of HIV and hepatitis B virus that acts as a synthetic cytidine analog. (cdc.gov)
- L'infection chronique par l'hépatite B, causée par le virus de l'hépatite B (VHB) et l'exposition aux aflatoxines est fondamentale dans la formation du CHC dans les pays en développement. (who.int)
- Cette revue de publications scientifiques vise à établir les effets néfastes des aliments contaminés par l'aflatoxine et met en évidence la corrélation entre l'aflatoxine et le carcinome hépatocellulaire associé au virus de l'hépatite B. La recherche a montré une augmentation significative de la survenue de CHC chez les personnes infectées par le VHB exposées à des toxines fongiques. (who.int)
Cancer3
- 1. Adenovirus-mediated expression of SSAT inhibits colorectal cancer cell growth in vitro. (nih.gov)
- 2. Adenovirus-mediated expression of both antisense ODC and AdoMetDC inhibited colorectal cancer cell growth in vitro. (nih.gov)
- 17. Polyamine catabolism in colorectal cancer cells following treatment with oxaliplatin, 5-fluorouracil and N1, N11 diethylnorspermine. (nih.gov)
Study1
- These cell lines were tested as part of another study ( 14 ), and the results confirmed as part of this study. (cdc.gov)
Entry1
- To explore the cellular entry mechanism of TFV, HepG2 cells were treated with drugs that inhibit the main endocytic pathways. (bvsalud.org)
Main1
- A condition that develops when your blood lacks enough healthy red blood cells which are the main transporters of oxygen to organs causing symptoms like fatigue. (cdc.gov)
Days1
- Macrophages were generated by treating CD14 + cells for 7 days with macrophage colony-stimulating factor and conditioned medium. (cdc.gov)