MiR-641 targets TMEFF2/MEK/PI3K to promote stem cell characteristics of pancreatic cancer cells

miR-641靶向TMEFF2/MEK/PI3K通路促进胰腺癌细胞干细胞特性。

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作者:Hongchao Han,Aikun Wang

Abstract

Background: Pancreatic cancer is a common malignant tumor. We focused on exploring the function of miR-641 in stem cell characteristics for pancreatic cancer cells. Method: MiR-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. Results: MiR-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. Conclusion: MiR-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. Supplementary Information: The online version contains supplementary material available at 10.1007/s12672-026-04584-2.

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