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

## TL;DR

This study shows that miR-641 promotes pancreatic cancer growth and stem cell traits by targeting TMEFF2/MEK/PI3K pathways.

## Contribution

The study identifies miR-641 as a novel oncogenic driver in pancreatic cancer by linking it to stem cell characteristics via TMEFF2/MEK/PI3K regulation.

## Key findings

- MiR-641 is overexpressed in pancreatic cancer tissues and correlates with poor patient survival.
- Knockdown of miR-641 reduces cancer cell proliferation, invasion, and stem-cell-like features in vitro and in vivo.
- MiR-641 promotes stem cell traits by targeting the TMEFF2/MEK/PI3K signaling pathway.

## Abstract

Pancreatic cancer is a common malignant tumor. We focused on exploring the function of miR-641 in stem cell characteristics for pancreatic cancer cells.

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.

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.

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.

The online version contains supplementary material available at 10.1007/s12672-026-04584-2.