On November 12, researcher Yang Juan and her workmates of GMU made breakthrough in the research on the molecular mechanism of liver cancer, and they published the research results entitled "TRIM11 Promotes Hepatocellular Carcinogenesis through Ubiquitin-proteasome Mediated Degradation of PHLPP1" on line in the international authoritative journal Hepatology (IF= 17.425). This study reveals that TRIM11 plays a carcinogenic role in liver cancer through PHLPP1/AKT signal pathway, suggesting that TRIM11 may be a promising target for the treatment of liver cancer. The GIITM and the First Affiliated Hospital of GMU (FAHGMU) are the first author units, and Professor Wang Xiangcai, director of the Oncology Department of SFCM, is the co-author of this paper.

This study finds that the expression of TRIM11 in HCC tissues is up-regulated compared with normal tissues. Over-expression of TRIM11 significantly promotes cell proliferation, migration and invasion in vitro and in vivo. Down-regulation of TRIM11 will have the opposite effect. In addition, the study also finds that TRIM11 participates in the occurrence and development of HCC by regulating the ubiquitination of PHLPP1, and thus activates the AKT signal pathway. The results show that TRIM11 is a key regulatory factor in the pathogenesis of HCC and may become a new potential target for HCC therapy.

Relevant link of the paper:

https://aasldpubs.onlinelibrary.wiley.com/doi/10.1002/hep.32234