AI Article Synopsis
- * Various experiments revealed that reducing DNTTIP2 levels led to cell cycle arrest in pancreatic cancer cells by impacting key proteins involved in cell proliferation.
- * The findings suggest that DNTTIP2 could be a promising target for therapies aimed at slowing down the progression of pancreatic cancer.
Article Abstract
Background/aim: Pancreatic cancer is one of the most lethal malignant cancers worldwide and the seventh most common cause of cancer-related death in both sexes. Herein, we analyzed open access data and discovered that expression of a gene called deoxynucleotidyltransferase terminal-interacting protein 2 (DNTTIP2) is linked to prognosis of pancreatic ductal adenocarcinoma (PDAC). We then elucidated the role of DNTTIP2 in the proliferation of pancreatic cancer cells in vitro.
Materials And Methods: A WST-8 assay, cell cycle analysis, Annexin-V staining, quantitative reverse transcription-PCR, and western blot analysis were conducted to assess cell proliferation, cell cycle, apoptosis, and expression of DNTTIP2 mRNA and protein, respectively, in DNTTIP2-depleteted MIA-PaCa-2 and PK-1 cells.
Results: Depletion of DNTTIP2 induced G arrest in MIA-PaCa-2 cells by decreasing expression of special AT-rich sequence binding protein 1 (SATB1) and cyclin-dependent kinase 6 (CDK6). In addition, depletion of DNTTIP2 induced G arrest in PK-1 cells by decreasing expression of CDK1. Depletion of DNTTIP2 did not induce apoptosis in MIA-PaCa-2 or PK-1 cells.
Conclusion: DNTTIP2 is involved in proliferation of pancreatic cancer cells. Thus, DNTTIP2 is a potential target for inhibiting progression of pancreatic cancers.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10756344 | PMC |
| http://dx.doi.org/10.21873/cgp.20426 | DOI Listing |
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