Department of Gastroenterology, Cangzhou Central Hospital, Cangzhou, Hebei 061000, China.
Dis Markers. 2022 Jul 19;2022:7594489. doi: 10.1155/2022/7594489. eCollection 2022.
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.
结直肠癌（CRC）是预后不良、死亡率高的侵袭性癌症之一。研究 CRC 的发病机制是为 CRC 提供有效诊断和预后策略的重中之重。COPS3 蛋白是 COP9 信号体（CSN）的一个亚基，与多种类型肿瘤的发生密切相关。然而，关于 COPS3 在结肠腺癌（COAD）中的作用的研究较少。本研究探讨了 COPS3 对结直肠癌细胞增殖、迁移和 EMT 的影响及其相关机制。COPS3 在 COAD 中高表达。COPS3 的缺失抑制了 COAD 细胞的活力并刺激了其凋亡。COPS3 的缺失抑制了 COAD 细胞的迁移和 EMT 过程。从机制上讲，我们发现 COPS3 可以介导 MEK/ERK 通路，从而影响 COAD 细胞的过程。我们认为 COPS3 可以作为一个有前途的 COAD 靶点。
