COLEC10: A potential tumor suppressor and prognostic biomarker in hepatocellular carcinoma through modulation of EMT and PI3K-AKT pathways.

Abstract

Hepatocellular carcinoma (HCC) is a cancer with poor prognosis, underscoring the urgent need for enhanced detection and management. This study aimed to investigate the role of Collectin Subfamily Member 10 (COLEC10) in HCC, which was revealed to be associated with various diseases. Bioinformatics tools, including GEO, cBioPortal, and TCGA, were used to identify differentially expressed genes. The prognostic significance of COLEC10 was assessed in two patient cohorts, and its functional impact on Hep3B and SMMC7721 cells was evaluated through CCK-8 and Transwell assays. The underlying mechanisms of COLEC10 in HCC progression were explored using flow cytometry and western blot. COLEC10 was downregulated in HCC and associated with poorer overall survival and disease progression. The potential interaction of COLEC10, CCBE1, and FCN3 was predicted. COLEC10, CCBE1, and FCN3 were identified as prognostic indicators for HCC. Overexpression of COLEC10 inhibited the proliferation, migration, and invasion of HCC cells. COLEC10 overexpression induced G0/G1 cell cycle arrest and suppressed epithelial-mesenchymal transition (EMT), COLEC10 regulated protein expression in the Hedgehog pathway and phosphorylation of key proteins in the PI3K-AKT pathway. COLEC10 is an independent prognostic factor of HCC. COLEC10 regulates EMT, Hedgehog, and PI3K-AKT pathways, providing new ideas for targeted therapy of HCC.