ArticleJournal of translational medicine2026
PAFAH1B1 stabilization, through PUM2-mediated competitive binding with miRNAs on its' 3'-UTR, takes active actions on ferroptosis to overcome the radioresistance to
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPancreatic cancer is one of the most fatal malignancies with the lowest 5-year survival worldwide. Radioresistance remains the major challenge for pancreatic cancer treatment. The aim of this study is to unravel the mechanism underlying PAFAH1B1-regulated radiosensitivity in pancreatic ductal adenocarcinoma (PDAC).
methodsImmunohistochemistry (IHC), western blot or qRT-PCR were employed to detect the expression of PAFAH1B1, PUM2 and other molecules. Two radiation-resistant (RR) PDAC cell lines and a xenograft mouse model were established. CCK-8, colony formation assays and flow cytometry analysis were used to assess cell proliferation and apoptosis in PDAC cells, respectively. Ferroptosis was evaluated using commercial kits and BODIPY 581/591 C11 staining. The association between PUM2 and PAFAH1B1 3'UTR, as well as between miR-421/miR-301a-3p and PAFAH1B1 3'UTR, were detected by luciferase and RNA immunoprecipitation (RIP) assays.
resultsPAFAH1B1 was downregulated in PDAC, and it was associated with unfavorable prognosis and radiotherapy response of PDAC patients. PAFAH1B1 overexpression enhanced the radiosensitivity to
conclusionPUM2/PAFAH1B1 axis decreased the radioresistance to
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