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Tripartite motif 52 (TRIM52) promotes proliferation, migration, and regulation of colon cancer cells associated with the NF-κB signaling pathway.

Background
With the advancement of early detection and treatment, the incidence of colon cancer (CC) has declined steadily worldwide; however, the mortality remains unacceptably high. Tripartite motif 52 (TRIM52) is a member of the family of highly conserved RBCC (a RING-finger, two B-boxes, and a predicted alpha-helical Coiled-Coil domain were linked to the N-terminal region in sequence) proteins with more than 70 isoforms, which plays an important role in tumorigenesis through different signaling pathways. How it regulates the development of CC remains unknown.


Methods
Western blot was used to reveal that TRIM52 protein expression is up-regulated in CC cells. The Analysis of The Cancer Genome Atlas (TCGA) database was used to find the different expressions of TRIM52 between colon cancer tissues and normal colonic epithelial tissues. Cell proliferation assays, migration and invasion assays, and apoptosis were used to verify the changes in cell function after knockdown or overexpression of TRIM52 in CC cells. After that, the key proteins of the nuclear factor (NF)-κB signaling pathway were validated by western blot to explore the role of TRIM52 in the NF-κB signaling pathway. Finally, in order to explore the potential sites of TRIM52, LPS and PDTC were employed to activate and block the NF-κB signaling pathway, and the key proteins of the NF-κB signaling pathway were validated by western blot.


Results
TGCA database revealed that TRIM52 expression was elevated in CC tissues and correlated with prognosis. It was verified that TRIM52 promoted the proliferation, migration, and invasion of CC cells, and inhibited cell apoptosis. Most of the tripartite motif proteins (TRIMs) have ubiquitin ligase activity related to their highly conserved RING structure. Detection of the key proteins of the NF-κB signaling pathway in CC cells revealed that TRIM52 activated the NF-κB signaling pathway.


Conclusions
We confirmed that TRIM52 promotes proliferation, migration, and invasion while inhibiting apoptosis of CC cells. The regulatory effect of TRIM52 on CC cells is related to the activation of the NF-κB signaling pathway. As TRIM52 acted as an upstream stimulator, stimulating the transfer of P65 into the nucleus to activate the NF-κB signaling pathway, it may provide a potential target for prognosis prediction and treatment of CC.