Chai Bao, Guo Yarong, Cui Xiangli, Liu Jinchun, Suo Yuhong, Dou Zhangfeng, Li Ning
Department of Gastroenterology, Shanxi Academy of Medical Science, Shanxi Dayi Hospital Taiyuan, Shanxi Province, China.
Department of Oncology, First Hospital of Shanxi Medical University Taiyuan, Shanxi Province, China.
Am J Transl Res. 2019 Jul 15;11(7):4516-4523. eCollection 2019.
Colon cancer is one of the most common malignancies worldwide, while the molecular mechanism remains largely unknown. miR-223-3p plays an important role in cancer development. Here, we found that miR-223-3p was up-regulated in 30 cases of colon cancer tissues as compared with their adjacent normal tissues. Lentivirus-mediated miR-223-3p over-expression promoted the proliferation, colony formation, migration and invasion of colon cancer cells. Inverse results were observed in miR-223-3p knockdown cells. Epithelial-mesenchymal transition (EMT) was regulated by miR-223-3p. In addition, cell apoptosis was suppressed and enhanced by miR-223-3p over-expression and knockdown, respectively. We further identified PRDM1, a tumor suppressor, was the target of miR-223-3p using microarray and luciferase assay. Our findings suggested that miR-223-3p acts as an oncogenic microRNA in colon cancer through regulating EMT and PRDM1.
结肠癌是全球最常见的恶性肿瘤之一,但其分子机制仍 largely 未知。miR - 223 - 3p 在癌症发展中起重要作用。在此,我们发现与相邻正常组织相比,30 例结肠癌组织中 miR - 223 - 3p 上调。慢病毒介导的 miR - 223 - 3p 过表达促进了结肠癌细胞的增殖、集落形成、迁移和侵袭。在 miR - 223 - 3p 敲低的细胞中观察到相反的结果。上皮 - 间质转化(EMT)受 miR - 223 - 3p 调控。此外,miR - 223 - 3p 过表达和敲低分别抑制和增强了细胞凋亡。我们使用微阵列和荧光素酶测定进一步鉴定出肿瘤抑制因子 PRDM1 是 miR - 223 - 3p 的靶标。我们的研究结果表明,miR - 223 - 3p 通过调节 EMT 和 PRDM1 在结肠癌中作为致癌性 microRNA 发挥作用。