TRIM72 inhibits cell migration and epithelial-mesenchymal transition by attenuating FAK/akt signaling in colorectal cancer

TRIM72 通过减弱结直肠癌中的 FAK/akt 信号传导来抑制细胞迁移和上皮-间质转化

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作者:Oluwasijibomi Damola Faleti, Yibing Gong, Jingyi Long, Qingshuang Luo, Haiqi Tan, Simin Deng, Lizhen Qiu, Xiaoming Lyu, Jinke Yao, Gongfa Wu

Abstract

TRIM72 (MG53), a membrane repair protein with E3-ligase activity, plays a crucial role in colorectal cancer (CRC). This study examined TRIM72 expression in primary CRC tumors and paired liver metastases using RT-PCR. Findings revealed significantly lower TRIM72 levels in liver metastases compared to primary tumors (p < 0.001). Aberrant TRIM72 expression correlated with lymph node metastasis and advanced clinical stages. Overexpression of TRIM72 inhibited CRC cell migration, intravasation, and EMT in vitro and in vivo, while TRIM72 knockout increased migration and invasion. TRIM72 interacted with Focal Adhesion Kinase (FAK), implicating the FAK/Akt signaling axis in colon cancer spread. Lower TRIM72 levels were associated with reduced survival rates, highlighting its potential as a prognostic marker and therapeutic target in CRC.

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