miR-106a对人结直肠癌SW480细胞增殖和侵袭能力的影响

目的：：研究 microRNA-106a(miR-106a)对低转移性人结直肠癌 SW480细胞增殖和侵袭等恶性生物学行为的影响。方法：采用实时荧光定量 PCR(quantitative real-time PCR,qRT-PCR)检测20对结直肠癌组织及其癌旁组织中 miR-106a的表达,将 miR-106a mimics 转染到 SW480细胞中,用 qRT-PCR法检测 miR-106a的表达水平,并用CCK8实验、克隆形成实验和划痕法检测 SW480细胞的增殖、克隆形成以及体外迁移能力。结果：与癌旁组织相比较,结直肠癌组织中 miR-106 a 的表达水平升高(t=2.05,P=0.047)；与mimics control转染组相比,miR-106a mimcs转染组miR-106a的表达水平显著升高(t=13.25,P=0.000),且细胞活力(72 h,t=4.52,P=0.000；96 h,t=6.17,P=0.000)和细胞克隆数明显升高(t=5.69,P=0.005),以及伤口愈合能力升高(48 h,t=5.44,P=0.032)。结论：过表达 miR-106a可显著促进低转移的人结直肠癌SW480细胞增殖和迁移能力,为结直肠癌的治疗提供了潜在的策略。

Effects of miR-106a on Invasion and Migration of Human Colorectal Cancer SW480 Cells

Objective:To explore the effect of microRNA-106a(miR-106a)on invasion and migration of human colorectal cancer(CRC) SW480 cells.Methods:First,real-time quantitative PCR was applied to detect the expression of miR-106a in 20 paired tumor tissues and cor-responding adjacent normal tissues.Then,miR-106a mimics or mimics control sequence(control group)were transfected into SW480 cells. Meanwhile,miR-106a abundance in SW480 cells was assessed by qRT-PCR before and after transfection.Then,cell proliferation and migration in mimics control group and miR-106a mimics group were assessed by CCK8 assay,clone formation assay,wound assay respectively.Results:The levels of miR-106a in colorectal cancer tissues were higher,compared with adjacent normal tissues(t=2.05,P=0.047).Compared with mimics control group,the abundance of miR-106a was significantly increased (t=13.25,P=0.000).Moreover,the proliferation was markedly promoted in miR-106a mimics group as compared in mimics control cells(72 h,t=4.52,P=0.000;96 h,t=6.17, P=0.000).The number of colonies formed was significantly increased(t=5.69,P=0.005)and so was migration capability in miR-106a mimics group cells as compared with mimics control cells(48 h,t=5.44,P=0.032).Conclusion:Over expression of miR-106a is capable of effectively promoting colorectal cancer cell proliferation and migration,which can provide a potential strategy for the therapy of CRC.