TRIM62 silencing represses the proliferation and invasion and increases the chemosensitivity of hepatocellular carcinoma cells by affecting the NF-κB pathway

Abstract

Tripartite interaction motif 62 (TRIM62), which is associated with the tumorigenic process, has been found to be aberrantly expressed in numerous cancers. However, the relationship between TRIM62 and hepatocellular carcinoma (HCC) has not been explored. In this work, the expression, function, and potential mechanism of TRIM62 in HCC were investigated. High TRIM62 levels were exhibited in HCC tissue, which contributed to a reduced overall survival. Loss-of-function experiments showed that TRIM62-silencing HCC cells proliferated more slowly, had reduced invasive ability and epithelial–mesenchymal transition, and were more sensitive to chemotherapeutic drug sorafenib. TRIM62 silencing resulted in the suppression of nuclear factor-kappa B (NF-κB), whereas the forced expression of TRIM62 enhanced NF-κB activation. The reduction of NF-κB could reverse TRIM62-overexpression-induced oncogenic effects in HCC cells. Importantly, TRIM62-silencing HCC cells had reduced tumorigenicity in nude mice. In summary, our data indicate that TRIM62 is highly expressed in HCC and acts as a potential tumor promoter. This work confirms that TRIM62 suppression displays remarkable tumor suppressive effects in HCC by affecting NF-κB activation.