ArticleAdvanced biomedical research2020
Investigation of the Effect of 5-Aza-2'-Deoxycytidine on p15INK4, p16INK4, p18INK4, and p19INK4 Genes Expression, Cell Growth Inhibition, and Apoptosis Induction in Hepatocellular Carcinoma PLC/PRF/5 Cell Line.
Article in Advanced biomedical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Microbiota-driven epigenetic modifications in gastrointestinal cancer: Implications for pathogenesis and therapeutic strategies.World journal of microbiology & biotechnology · 2025Review
- AssessingNuclear medicine and molecular imaging · 2025Article
- The efficacy of sorafenib against hepatocellular carcinoma is enhanced by 5-aza-mediated inhibition of ID1 promoter methylation.FEBS open bio · 2024Article
- The Effect of 5-aza,2'-deoxyCytidine (5 AZA CdR or Decitabine) on Extrinsic, Intrinsic, and JAK/STAT Pathways in Neuroblastoma and Glioblastoma Cells Lines.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Effect of 5'-Fluoro-2'-Deoxycytidine and Sodium Butyrate on the Gene Expression of the Intrinsic Apoptotic Pathway, p21, p27, and p53 Genes Expression, Cell Viability, and Apoptosis in Human Hepatocellular Carcinoma Cell Lines.Advanced biomedical research · 2023Article
- Effect of Sodium Butyrate and Epigallocatechin-3-Gallate on the Genes Expression of Intrinsic Apoptotic Pathway on PA-TU-8902, CFPAC-1, and CAPAN-1 Human Pancreatic Cancer Cell Lines: Epi-drugs and Intrinsic Apoptotic Pathway in Pancreatic Cancer.Galen medical journal · 2022Article
- Histone Deacetylase Inhibitors, Intrinsic and Extrinsic Apoptotic Pathways, and Epigenetic Alterations of Histone Deacetylases (HDACs) in Hepatocellular Carcinoma.Iranian journal of pharmaceutical research : IJPR · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCyclin-dependent kinases (CDKs) are the key regulators of cell-cycle transitions and characterized by needing a separate subunit, a cyclin, which provides domains essential for enzymatic activity. The activities of cyclin-CDK complexes are controlled by a group of molecules that inhibit CDK activity and CDK inhibitors (CKIs). Cancer often exhibits an aberrant CpG methylation of promoter regions of tumor suppressor genes such as CKIs. Treatment with the DNA demethylating agents, such as 5-aza-2'-deoxycytidine (5-Aza-CdR), can restore and upregulate CKIs. Previously, we reported the effect of 5-Aza-CdR and genistein on DNA methyltransferase (DNMTs) in hepatocellular carcinoma (HCC). The aim of the present study was to evaluate the effect of 5-Aza-CdR on p15INK4, p16INK4, p18INK4, and p19INK4 genes expression, cell growth inhibition, and apoptosis induction in HCC PLC/PRF/5 cell line. MATERIALS AND
methodsThe effect of 5-Aza-CdR on the cell growth of PLC/PRF/5 cells, genes expression, and apoptosis induction were assessed by 3-[4, 5-dimethyl-2-thiazolyl]-2, 5-diphenyl-2H-tetrazolium bromide assay, real-time quantitative reverse transcription-polymerase chain reaction analysis, and flow cytometry, respectively.
results5-Aza-CdR (0, 1, 5, 10, 25, and 50 μM) inhibited PLC/PRF/5 cell growth at different periods significantly. This compound induced apoptosis and reactivated p15INK4, p16INK4, p18INK4, and p19INK4 genes expression at a concentration of 5 μM significantly.
conclusion5-Aza-CdR can inhibit cell viability and induce apoptosis by epigenetic reactivation of p15INK4, p16INK4, p18INK4, and p19INK4 genes in HCC PLC/PRF/5.
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