Zhao Hongjian, Huang Junjun, Chen Ming, Li Baoru, Chen Xinran, Zhou Mingqing
Department of General Surgery, Zhabei Central Hospital of Jing'an District, Shanghai, China.
Front Oncol. 2021 Sep 13;11:695525. doi: 10.3389/fonc.2021.695525. eCollection 2021.
Colorectal cancer (CRC) is one of the leading causes of cancer death worldwide, with most mortalities being caused by metastases. However, the underlying molecular mechanism of CRC metastases remains largely unknown. Emerging evidence has shown the role of the tripartite motif family, especially tripartite motif protein 6 (TRIM6), in carcinogenesis. In this study, we used CRC cell lines with TRIM6 knockdown and overexpression to investigate the function of TRIM6 in CRC metastasis. We found that TRIM6 promotes CRC cell migration and invasion both and . TRIM6 knockdown slows down the migration and invasion processes, whereas TRIM6 overexpression accelerates CRC cell migration and invasion. TRIM6 is potentially the upstream regulatory factor for signal transducer and activator of transcription 3 (STAT3) the suppressor of cytokine signaling 2 (SOCS2). A total of 70 samples from patients with CRC further confirmed that TRIM6 expression level is positively correlated with STAT3 phosphorylation and negatively correlated with SOCS2 expression. Therefore, TRIM6 could be a potential therapeutic target for CRC metastasis.
结直肠癌(CRC)是全球癌症死亡的主要原因之一,大多数死亡是由转移引起的。然而,CRC转移的潜在分子机制在很大程度上仍然未知。新出现的证据表明了三重基序家族,特别是三重基序蛋白6(TRIM6)在致癌作用中的作用。在本研究中,我们使用了TRIM6敲低和过表达的CRC细胞系来研究TRIM6在CRC转移中的功能。我们发现TRIM6在体内和体外均促进CRC细胞迁移和侵袭。TRIM6敲低减缓了迁移和侵袭过程,而TRIM6过表达加速了CRC细胞迁移和侵袭。TRIM6可能是信号转导和转录激活因子3(STAT3)——细胞因子信号抑制因子2(SOCS2)的上游调节因子。来自CRC患者的70个样本进一步证实,TRIM6表达水平与STAT3磷酸化呈正相关,与SOCS2表达呈负相关。因此,TRIM6可能是CRC转移的潜在治疗靶点。