ArticleCell proliferation2014
Inhibition enhancer of zeste homologue 2 promotes senescence and apoptosis induced by doxorubicin in p53 mutant gastric cancer cells.
Article in Cell proliferation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
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- Development and validation of a patient-specific model to predict postoperative SIRS in older patients: A two-center study.Frontiers in public health · 2023Article
- Review
- B7-H3 suppresses doxorubicin-induced senescence-like growth arrest in colorectal cancer through the AKT/TM4SF1/SIRT1 pathway.Cell death & disease · 2021Article
- Creatine Alleviates Doxorubicin-Induced Liver Damage by Inhibiting Liver Fibrosis, Inflammation, Oxidative Stress, and Cellular Senescence.Nutrients · 2020Article
- Targeting epigenetics in sarcomas through EZH2 inhibition.Journal of hematology & oncology · 2020Article
- Curcumin inhibits liver metastasis of gastric cancer through reducing circulating tumor cells.Aging · 2019Article
- EZH2 promotes hepatocellular carcinoma progression through modulating miR-22/galectin-9 axis.Journal of experimental & clinical cancer research : CR · 2018Article
- Epigenetic Contribution of High-Mobility Group A Proteins to Stem Cell Properties.International journal of cell biology · 2018Review
- Naringin protects myocardial cells from doxorubicin‑induced apoptosis partially by inhibiting the p38MAPK pathway.Molecular medicine reports · 2017Article
- EZH2-mediated repression of Dkk1 promotes hepatic stellate cell activation and hepatic fibrosis.Journal of cellular and molecular medicine · 2017Article
- Initial testing (stage 1) of tazemetostat (EPZ-6438), a novel EZH2 inhibitor, by the Pediatric Preclinical Testing Program.Pediatric blood & cancer · 2017Article
- EZH2-mediated repression of GSK-3β and TP53 promotes Wnt/β-catenin signaling-dependent cell expansion in cervical carcinoma.Oncotarget · 2016Article
- MiR-330-3p inhibits gastric cancer progression through targeting MSI1.American journal of translational research · 2016Article
- Retinoblastoma-binding Protein 4-regulated Classical Nuclear Transport Is Involved in Cellular Senescence.The Journal of biological chemistry · 2015Article
- DZNep inhibits the proliferation of colon cancer HCT116 cells by inducing senescence and apoptosis.Acta pharmaceutica Sinica. B · 2015Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesEnhancer of zeste homologue 2 (EZH2) is crucially involved in epigenetic silencing by acting as a histone methyltransferase. Although EZH2 is overexpressed in many cancers and is involved in malignant cell proliferation and invasion, the role of EZH2 in senescence induced by DNA damage has up to now remained largely unknown. In this study, we sought to explore the outcome of EZH2 depletion along with exposure of doxorubicin (DOX), and related mechanisms, in gastric cancer cells. MATERIALS AND
methodsHere, senescence induced by DNA damage was achieved in gastric cancer cells by DOX treatment. EZH2 was downregulated by transfection with siRNA or treated with (-)-epigallocatechin-3-gallate, a targeted inhibitor. Senescence-associated β galactosidase (SA-β-gal) and formation of senescence-associated heterochromatin foci were used to identify cell senescence. To investigate effects of EZH2 depletion on the cell cycle, apoptosis and proliferation, flow cytometry and MTT analysis were employed. Changes in p53-p21 axis activation were detected by Western blotting.
resultsWe found that cell proliferative arrest caused by DOX could be promoted by EZH2 depletion. Mechanistically, EZH2 depletion not only worked in coordination with DNA damage during the progression of cell senescence but also promoted apoptosis in p53 mutant cells. However, it had no cooperative relationship with DOX in p53 wild-type cells.
conclusionsThese data help unravel a crucial role for EZH2 in senescence and apoptosis in gastric cancer cells and that p53 genomic status was associated with different cell responses to EZH2 silencing.
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