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目的探讨miR-338-5p在结直肠癌组织中的表达状况,以及miR-338-5p过表达对结肠癌细胞系HCT116和SW620增殖、凋亡及细胞周期的影响。方法使用实时定量PCR方法检测miR-338-5p在40例临床诊断为结直肠癌患者配对癌组织及癌旁组织中的表达情况。随后使用miR-338-5p-mimics转染结肠癌细胞系HCT116和SW620,确认过表达成功后,分别使用CCK-8法、FITC-AnnexinⅤ-PI法及Propidium iodide法检测肿瘤细胞的增殖、凋亡和细胞周期的改变。结果①miR-338-5p在结直肠癌组织中的表达明显低于其在相应的癌旁组织中的表达(P<0.01)。②与转染阴性对照比较,转染miR-338-5p-mimics后,HCT116和SW620细胞增殖能力明显减弱(P<0.01),凋亡率明显增加〔HCT116细胞:(11.43±0.67)%比(7.98±0.36)%,P<0.01;SW620细胞:(10.5±0.2)%比(7.93±0.5)%,P<0.01〕,诱导HCT116和SW620细胞G1期阻滞〔HCT116细胞:(80.41±1.34)%比(64.87±1.83)%,P<0.01;SW620细胞:(68.76±0.41)%比(54.89±0.78)%,P<0.01〕。结论 miR-338-5p可能作为抑癌基因在结直肠癌中发挥作用,并对细胞增殖、凋亡和周期有显著影响。
Objective To investigate the expression of miR-338-5p in colorectal cancer tissues and the effect of miR-338-5p overexpression on the proliferation, apoptosis and cell cycle of colon cancer cell lines HCT116 and SW620. Methods Real-time PCR was used to detect the expression of miR-338-5p in matched cancer tissues and paracancerous tissues of 40 patients with clinically diagnosed colorectal cancer. Subsequently, the colon cancer cell lines HCT116 and SW620 were transfected with miR-338-5p-mimics. After successful overexpression, the CCK-8 assay, FITC-Annexin V-PI assay, and Propidium iodide assay were used to detect tumor cell proliferation and apoptosis. And changes in the cell cycle. Results The expression of miR-338-5p in colorectal cancer tissue was significantly lower than that in the corresponding adjacent tissue (P<0.01). 2 Compared with transfected negative control, after transfection with miR-338-5p-mimics, the proliferation ability of HCT116 and SW620 cells was significantly decreased (P<0.01), and the apoptosis rate was significantly increased [HCT116 cells: (11.43±0.67)% ratio ( 7.98±0.36)%, P<0.01; SW620 cells: (10.5±0.2)% vs. (7.93±0.5)%, P<0.01), induced G1 arrest of HCT116 and SW620 cells [HCT116 cells: (80.41±1.34) % (64.87±1.83)%, P<0.01; SW620 cells: (68.76±0.41)% vs. (54.89±0.78)%, P<0.01). Conclusion miR-338-5p may play a role as a tumor suppressor gene in colorectal cancer, and has a significant effect on cell proliferation, apoptosis and cycle.