ArticleMolecular medicine reports2012
Reduced levels of p15INK4b, p16INK4a, p21cip1 and p27kip1 in pancreatic carcinoma.
Article in Molecular medicine reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Clinicopathological Significance of CDKN2A Promoter Hypermethylation Frequency with Pancreatic Cancer.Scientific reports · 2015Pooled it
- Investigating the Impact of the Secretome From hAMSCs on HT-29 Colon Cancer Cells via TNF-α/TGF-β/c-MYC Signaling Pathways Using a Three-Dimensional Cell Culture Model.Immunity, inflammation and disease · 2025Article
- Effect of Sodium Butyrate on p16INK4a, p14ARF, p15INK4b, Class I HDACs (HDACs 1, 2, 3) Class II HDACs (HDACs 4, 5, 6), Cell Growth Inhibition and Apoptosis Induction in Pancreatic Cancer AsPC-1 and Colon Cancer HCT-116 Cell Lines.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Effect of vorinostat on INK4 family and HDACs 1, 2, and 3 in pancreatic cancer and hepatocellular carcinoma.Research in pharmaceutical sciences · 2021Article
- Investigation of the Effect of 5-Aza-2'-Deoxycytidine in Comparison to and in Combination with Trichostatin A onInternational journal of preventive medicine · 2021Article
- A DNA Hypomethylating Drug Alters the Tumor Microenvironment and Improves the Effectiveness of Immune Checkpoint Inhibitors in a Mouse Model of Pancreatic Cancer.Cancer research · 2020Article
- 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.Advanced biomedical research · 2020Article
- Effect of Zebularine on p16INK4a, p14ARF, p15INK4b, and DNA Methyltransferase 1 Gene Expression, Cell Growth Inhibition, and Apoptosis Induction in Human Hepatocellular Carcinoma PLC/PRF5 and Pancreatic Cancer PA-TU-8902 Cell Lines.Iranian journal of pharmaceutical research : IJPR · 2020Article
- Deciphering DNA methylation signatures of pancreatic cancer and pancreatitis.Clinical epigenetics · 2019Review
- TET1-mediated DNA hydroxymethylation activates inhibitors of the Wnt/β-catenin signaling pathway to suppress EMT in pancreatic tumor cells.Journal of experimental & clinical cancer research : CR · 2019Article
- Long non-coding RNA SNHG15 inhibits P15 and KLF2 expression to promote pancreatic cancer proliferation through EZH2-mediated H3K27me3.Oncotarget · 2017Article
- Expression of the tumor suppressor gene p16, and lymph node metastasis in patients with ovarian cancer.Oncology letters · 2017Article
- Long non-coding RNA IRAIN suppresses apoptosis and promotes proliferation by binding to LSD1 and EZH2 in pancreatic cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Cell-free DNA promoter hypermethylation in plasma as a diagnostic marker for pancreatic adenocarcinoma.Clinical epigenetics · 2016Observational
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic carcinoma is one of the leading causes of cancer mortality worldwide, although the molecular mechanisms of this disease are poorly understood. The aim of this study was to examine the expression of cyclin-dependent kinase inhibitors (CDKIs) and the epigenetic modifications in the promoters of these genes. We also evaluated the correlation between the methylation status of CDKI genes and smoking habit in clinical pancreatic carcinoma specimens. Western blotting and real-time PCR were performed to assess CDKI expression. Methylation-specific PCR was carried out to examine the methylation status of the promoters of CDKI genes. In this study, we revealed that reduced levels of the CDKI proteins, p15INK4b, p16INK4a, p21cip1 and p27kip1, are a prominent feature of pancreatic carcinoma patients. The DNA hypermethylation of the promoter was observed in 40% (2 of 5) of the p15INK4b genes, 60% (3 of 5) of the p16INK4a genes and 60% of the p21cip1 genes, which markedly correlated with their decreased mRNA expression. No hypermethylation was detected in the p27kip1 gene promoter in 5 pancreatic carcinoma patients with markedly decreased expression of p27kip1 mRNA, suggesting an alternative mechanism of p27kip in these patients. In this study, patients with a smoking habit displayed methylation of 2 CDKI genes in their pancreatic carcinoma specimens. We concluded that epigenetic modification via hypermethylation represents a critical mechanism for the inactivation of CDKI genes in pancreatic carcinoma.
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