ArticleDiscover oncology2026
MiR-641 targets TMEFF2/MEK/PI3K to promote stem cell characteristics of pancreatic cancer cells.
Article in Discover oncology, 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 a common malignant tumor. We focused on exploring the function of miR-641 in stem cell characteristics for pancreatic cancer cells.
methodMiR-641 expression was analyzed based on The Cancer Genome Atlas (TCGA) pancreatic cancer database and clinical samples. The miR-641 knockdown within pancreatic cancer was performed by cell transfection. CCK8, transwell, and flow cytometry were performed for analyzing cell growth, invasion as well as stem-cell-like features separately. Meanwhile, this study carried out the dual luciferase reporter gene assay. In vivo xenograft tumor assay was also performed.
resultsMiR-641 expression increased in clinical pancreatic cancer tissues and cells compared with normal cells. MiR-641 predicted poor survival rate of pancreatic cancer patients. MiR-641 down-regulation inhibited pancreatic cancer cell proliferation, clone forming ability, invasion and migration. Down-regulation of miR-641 inhibited the capability of sphere-forming, reduced CD133 + and CD44 + cell quantities, and suppressed CD133, CD44, and Oct4 expression in Down-regulation of miR-641 cells. MiR-641 targeted TMEFF2/MEK/PI3K for promoting pancreatic cancer cells’ stem-cell-like characteristics. MiR-641 also promoted tumor growth in vivo.
conclusionMiR-641 acts as an oncogene that promotes pancreatic cancer cell growth, invasion as well as stem-cell-like features, which is realized by regulating the expression of TMEFF2.
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