SPOCK1 promotes the proliferation and migration of colon cancer cells by regulating the NF-κB pathway and inducing EMT.

Abstract

Sparc/osteonectin, cwcv, and kazal-like domains proteoglycan 1 (SPOCK1) has been shown to promote various tumors, but its role in colon cancer (CRC) has not been clearly illuminated. The aim of this study was to investigate the effects of SPOCK1 interference on the proliferation, migration, and EMT of CRC cells. First, we analyzed the expression of SPOCK1 in various CRC datasets. Then, we investigated the correlation between SPOCK1 and prognosis in CRC patients. We overexpressed SPOCK1 and knocked down SPOCK1 expression in HCT-116 and SW480 cells, respectively. Then, cell proliferation was assayed with a CCK-8 assay, and cell migration was evaluated with a Transwell migration assay. NF-κB and EMT-related proteins were studied by western blotting. The results indicated that the mRNA levels of SPOCK1 were relatively high in CRC tissues and that high expression of SPOCK1 was negatively correlated with patient prognosis. With SPOCK1 overexpression in HCT-116 cells, cell proliferation and migration were increased, while SPOCK1 knockdown had the opposite effects. With SPOCK1 overexpression in HCT-116 cells, the expression levels of NF-κB and EMT-related proteins were elevated, while SPOCK1 knockdown produced the opposite results. In conclusion, our study demonstrates that SPOCK1 may activate the NF-κB/Snail signaling cascade to promote the proliferation and migration of CRC cells. SPOCK1 may serve as a new prognostic indicator and potential therapeutic target in CRC.