TRIM29 facilitates proliferation and malignancy of cholangiocarcinoma cells by activating MAPK and β-catenin pathways.

Abstract

Tripartite motif-containing 29 (TRIM29) has been found to be involved in the regulation of cancer progression and its function varies depending on the type of cancer. However, the role of TRIM29 in cholangiocarcinoma has yet to be revealed. This study initially explored the role of TRIM29 in cholangiocarcinoma. TRIM29 expression in cholangiocarcinoma cells were scrutinized by quantitative real-time reverse transcription polymerase chain reaction and Western blot. The function of TRIM29 on cholangiocarcinoma cell viability, proliferation, migration and sphere formation abilities were studied by cell count kit-8, clone formation, Transwell and sphere formation assays. TRIM29 effect on the expression of proteins associated with epithelial-mesenchymal transition and cancer stem cell characteristics were researched by Western blot. TRIM29 effect on MAPK and β-catenin pathway activity was researched through Western blot. TRIM29 was overexpressed in cholangiocarcinoma cells. TRIM29 silencing mitigated the viability, proliferation, migration and sphere formation abilities of cholangiocarcinoma cells, increased E-cadherin expression and decreased the expression of N-cadherin, Vimentin, CD33, Sox2 and Nanog proteins in cholangiocarcinoma cells. The loss of TRIM29 suppressed the expression of p-MEK1/2/MEK1/2 and p-ERK1/2/ERK1/2 in cholangiocarcinoma cells. The inhibition of the MAPK and β-catenin signaling pathways abrogated the promotion of TRIM29 on cholangiocarcinoma cell viability, proliferation, migration, EMT, and cancer stem cell characteristics. TRIM29 plays an oncogenic role in cholangiocarcinoma. It may promote the malignancy of cholangiocarcinoma via inducing the activation of the MAPK and β-catenin pathways. Thus, TRIM29 may aid in the creation of innovative treatment strategies for cholangiocarcinoma.