ArticleTranslational cancer research2025
MicroRNA-125b inhibits apoptosis and increases gemcitabine resistance by downregulating the expression of BAK1 in pancreatic ductal adenocarcinoma.
Article in Translational cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Liquid biopsy-based epigenetic signatures for early detection of prostate cancer: a systematic review.Frontiers in oncology · 2026Pooled it
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Authors and funding
6 authors.
Funding
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Abstract
Background: Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies due to its aggressive progression and poor prognosis. Chemotherapy with gemcitabine is a standard treatment, yet the development of resistance severely limits gemcitabine effectiveness. Understanding the molecular mechanisms underlying this resistance is thus crucial for improving therapeutic outcomes. This study investigated the roles of microRNA-125b (miR-125b) in PDAC, focusing on its influence on cell proliferation and gemcitabine resistance. Methods: We employed quantitative real-time polymerase chain reaction (qRT-PCR) to measure miR-125b levels in PDAC tissues and cell lines, and utilized cell proliferation assays, apoptosis assays, and luciferase reporter assays to elucidate miR-125b's functions and targets. Finally, the Results: MiR-125b was found to be significantly overexpressed in PDAC tissues and cell lines. Overexpression of miR-125b promoted cell proliferation by enhancing cell cycle progression and reducing apoptosis in response to gemcitabine and nutrient starvation. Luciferase reporter assays identified Bcl-2 homologous antagonist/killer 1 (BAK1), a pro-apoptotic protein, as a direct target of miR-125b. Downregulation of Conclusions: In summary, our study indicated that miR-125b contributes to PDAC progression and gemcitabine resistance by downregulating
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