MiR-671-3p通过CKAP4抑制结肠癌细胞的增殖和迁移

MicroRNA-671-3p inhibits the proliferation and migration of colon cancer throgh CKAP4

目的探讨miR-671-3p对结肠癌体外生物学特性的影响及其机制。方法体外培养结肠癌RKO和SW620细胞株,转染miR-671-3p的过表达片段和抑制剂,qRT-PCR检测细胞的过表达效率和干扰效率。CCK-8实验检测体外培养细胞的增殖能力,Transwell实验检测体外细胞的迁移能力。生物信息学方法分析CKAP4在结肠癌细胞的表达。结果在RKO和SW620细胞中过表达miR-671-3p,细胞的体外迁移能力显著降低(RKO细胞:P<0.001;SW620细胞:P=0.004),增殖能力明显下降(RKO细胞:P=0.032;SW620细胞:P=0.012),而干扰miR-671-3p后则表现出相反的结果。另外,miR-671-3p的下游靶基因CKAP4在结肠癌表达增高,但对其生存时间无影响。体外过表达CKAP4能够逆转miR-671-3p所导致的抑制的迁移能力和增殖能力。结论miR-671-3p通过CKAP4可以有效抑制体外结肠癌细胞的增殖能力和迁移能力,提示其在结肠癌的发展进程中发挥着重要的作用。

Objective To explore the functional role and underlying mechanisms of miR-671-3p in colon cancer cell proliferation and migration in vitro.Methods MiR-671-3p mimics and its inhibitor were transfected into RKO and SW620 cells,respectively.Fluorescence quantitative PCR was used to assess the interference or over-express efficiency after transfection of miR-671-3p mimics or inhibitor.A Boyden chamber assay was used to detect the cell migration abilities of cells.CCK-8 assay was used to assess the cell proliferation abilities;meanwhile,a Boyden chamber assay was aimed to detect the cell migration ability.The expression of the downstream target of miR-671-3p was analyzed by bioinformatics methods.Results Data showed that forced expression of miR-671-3p inhibited the proliferation and migration in RKO and SW620 cells,respectively.By contrast,inhibition of miR-671-3p reached the opposite effects.Moreover,CKAP4 was upregulated in conlon cancer,which was not related to the survival time of the patients.Ectopic expression of CKAP4 reversed the migration and proliferation suppressive activity induced by miR-671-3p on CRC cells.Conclusion Our study showed that miR-671-3p inhibits migration and proliferation via CKAP4 in colon cancer cells in vitro,indicating it plays an important role in progression of CRC.