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

被引：0
作者：
Faleti, Oluwasijibomi Damola [1 ,2 ]
Gong, Yibing [1 ]
Long, Jingyi [1 ]
Luo, Qingshuang [1 ]
Tan, Haiqi [1 ]
Deng, Simin [1 ]
Qiu, Lizhen [3 ]
Lyu, Xiaoming [1 ]
Yao, Jinke [4 ]
Wu, Gongfa [5 ]
机构：
[1] Southern Med Univ, Affiliated Hosp 3, Dept Lab Med, Guangzhou 510630, Guangdong, Peoples R China
[2] Hong Kong Polytech Univ, Dept Appl Biol & Chem Technol, Hong Kong 999000, Peoples R China
[3] Guangzhou Med Univ, Affiliated Hosp 4, Hlth Management Ctr, Guangzhou 511300, Guangdong, Peoples R China
[4] Guangzhou Med Univ, Affiliated Hosp 4, Dept Gen Surg, Guangzhou 511300, Guangdong, Peoples R China
[5] Guangzhou Med Univ, Affiliated Hosp 4, Dept Pathol, Guangzhou 511300, Guangdong, Peoples R China
来源：
HELIYON | 2024年 / 10卷 / 18期
关键词：
TRIM72; Migration; Epithelial-mesenchymal transition; FAK/Akt; Colorectal cancer; FOCAL ADHESION KINASE; EXTRACELLULAR-MATRIX; LUNG-CANCER; E-CADHERIN; REPAIR; METASTASIS; PROTEINS; PROMOTES;
D O I：
10.1016/j.heliyon.2024.e37714
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
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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收藏
页数：10
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