Colorectal cancer (CRC) is one of the most aggressive cancers with poor prognosis and high mortality. The study of the pathogenesis of CRC is a top priority in providing effective diagnostic and prognostic strategies for CRC. COPS3 protein is a subunit of the COP9 signaling body (CSN), which is closely associated with the development of multiple types of tumors. However, there are few studies on the role of COPS3 in colon adenocarcinoma (COAD). This study investigated the effects of COPS3 on proliferation, motility, and EMT of colorectal cancer cells and related mechanisms. COPS3 was highly expressed in COAD. The depletion of COPS3 suppressed the viability and stimulated the apoptosis of COAD cells. Depletion of COPS3 suppressed the motility and EMT process of COAD cells. Mechanically, we found that COPS3 could mediate MEK/ERK pathway and therefore affected the process of COAD cells. We thought that COPS3 could serve as a promising COAD target.

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