Inhibitory Effect and Mechanism of the Down-Regulation of TRIM32 in Colorectal Cancer

TRIM32 protein represents a crucial member of TRIM family that is highly expressed in numerous human cancers, and is associated with a poor prognosis. However, the mechanism of TRIM32 in colorectal cancer (CRC) is unclear. The expression of TRIM32 and its prognostic value in CRC were analyzed using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database. Real-time quantitative PCR, immunohistochemistry (IHC), and cell proliferation assays were used to explore the effects of down-regulation of TRIM32 expression on the proliferation, migration, and apoptosis of cultured CRC cells (HCT116 and SW480 cells) and in xenogeneic tumorigenic animals. Bioinformatics analysis showed that TRIM32 is up-regulated in many types of cancers, and exhibits significant prognostic value in CRC. Western blotting results showed that after knocking down TRIM32, the expression level of IκBα increased, and the expression levels of TRIM32, p-p65, Bcl-2, and IKKβ decreased. The inhibitory effect of TRIM32 on CRC in vivo was evaluated by measuring tumor volume and weight, Hematoxylin and eosin (H&E) staining, and Ki67 IHC staining in heterotopic tumor-forming mice with CRC. Down-regulation of TRIM32 can inhibit the activation of the NF-κB signaling pathway and the occurrence of CRC. Our research provides a new insight into the pathogenesis of CRC, and a therapeutic target for the treatment of CRC.