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.

Hepatocellular carcinoma (HCC) is characterized by a poor prognosis because of its insensitivity to radiation and chemotherapy. Recently, circular RNAs (circRNAs) have been found to serve important roles in hepatocellular carcinogenesis. circ‑CCT3, a novel circRNA, was screened from the differential tissue expression results of a circRNA microarray. Relative expression levels of circ‑CCT3 in specimens and cell lines were evaluated by reverse transcription‑quantitative PCR and the relationship between circ‑CCT3 and prognosis was analyzed by Kaplan‑Meier curves. The oncogenic role of circ‑CCT3 was confirmed in HCC cells through a cell counting kit‑8 (CCK‑8) assay, a colony formation assay, acridine orange/ethidium bromide double fluorescence staining, flow cytometry, a wound‑healing assay and a Transwell assay. Bioinformatics prediction and luciferase reporter assays validated that circ‑CCT3 facilitated HCC progression through the miR‑1287‑5p/TEA domain transcription factor 1 (TEAD1) axis. TEAD1 could then directly activate patched 1 and lysyl oxidase transcription, as analyzed by chromatin immunoprecipitation and luciferase reporter assays. The present study identified a novel circRNA, circ‑CCT3, which may be used as a potential therapeutic target for HCC.