ArticleMolecular medicine reports2018
DNA methyltransferase 3a modulates chemosensitivity to gemcitabine and oxaliplatin via CHK1 and AKT in p53‑deficient pancreatic cancer cells.
Article in Molecular medicine reports, 2018. 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.
- DNMT3A in cancer: from epigenetic writer to oncogenic driver.Clinical epigenetics · 2026Review
- Oxaliplatin resistance in pancreatic ductal adenocarcinoma is non‑significantly mediated by diminished drug uptake but is highly linked to a poor apoptotic response to the cytotoxic threat.Oncology reports · 2026Article
- Prevalence and clinical relavance of germline mutations in Chinese patients with pancreatic cancer.Cell communication and signaling : CCS · 2025Article
- Hsa_circ_0084003 modulates glycolysis and epithelial-mesenchymal transition in pancreatic ductal adenocarcinoma through targeting hsa-miR-143-3p/DNMT3A axis.Toxicology research · 2023Article
- An Overview of Epigenetic Methylation in Pancreatic Cancer Progression.Frontiers in oncology · 2022Review
- Article
- PD-L1 upregulation accompanied with epithelial-mesenchymal transition attenuates sensitivity to ATR inhibition in p53 mutant pancreatic cancer cells.Medical oncology (Northwood, London, England) · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aberrant expression of DNA methyltransferases (DNMTs) has been considered to be associated with pancreatic carcinogenesis and progression. DNMT3a is widely involved in cell proliferation and cell cycle progression in pancreatic ductal adenocarcinoma (PDAC) cells. However, its regulation of chemosensitivity to gemcitabine (GEM) and oxaliplatin (OXA) in p53‑deficient PDAC remains unclear. In the present study, the effect and mechanisms of DNMT3a on GEM and OXA chemosensitivity in p53‑deficient PDAC cells were investigated using MTT assay, cell cycle analysis, apoptosis analysis and western blotting. The treatment of GEM and OXA induced S phase arrest by DNA damage, and enhanced the activation of the AKT signaling pathway in Panc‑1 cells. Downregulation of DNMT3a increased the chemosensitivity to both GEM and OXA in Panc‑1 cells. DNMT3a depletion distinctly abolished S phase arrest induced by GEM and OXA. Further research demonstrated that activation inhibition of CHK1 and AKT, as well as an increase in apoptosis, were involved in DNMT3a‑mediated chemosensitivity to GEM and OXA. Taken together, these data demonstrated that DNMT3a serves a crucial role in the regulation of chemosensitivity to GEM and OXA, and suggests a promising therapeutic target for p53‑deficient PDAC.
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