miR-766-5p 过表达介导 MMP-7 对胶质瘤细胞增殖、 侵袭与凋亡的影响及机制

目的 探讨 miR-766-5p 对胶质瘤细胞增殖、 侵袭与凋亡的影响。 方法 Targetscan 预测 miR-766-5p 与基质金属蛋白酶-7 (MMP-7) 靶向关系并进行验证, 构建 miR-766-5p 过表达、 MMP-7 过表达和 miR766-5p + MMP-7 过表达胶质瘤 U87 细胞系, BrdU 染色、 流式细胞法、 Transwell 实验、 Western 印迹分别检测细胞增殖、 凋亡、 侵袭及相关蛋白表达。 结果 miR-766-5p 可靶向抑制 MMP-7 表达, miR-766-5p 过表达可抑制 Ki67、 增殖细胞核抗原 (PCNA)、 Wnt1、 β-链蛋白 (β-catenin) 蛋白表达以抑制 U87 细胞增殖和侵袭, 可促进 Bcl 相关 X 蛋白 (Bax) / B 细胞淋巴瘤/ 白血病-2 (Bcl-2) 蛋白表达以促进细胞凋亡, MMP-7过表达可以缓解 miR-766-5p 过表达所致 U87 细胞增殖、 侵袭抑制作用和凋亡促进作用。 结论 miR-766-5p可靶向抑制 MMP-7 表达抑制 U87 细胞胞增殖、 侵袭和促细胞凋亡。

Effect of miR-766-5p Overexpression Mediated MMP-7 Inhibition onthe Proliferation,Invasion and Apoptosis of Glioma Cells

Objective To explore the effect of miR-766-5p on the proliferation, invasion andapoptosis of glioma cells. Methods The targeting relationship between miR-766-5p and matrix metalloproteinase-7 (MMP-7) was predicted by Targetscan, and then was verified. U87 cell lines withmiR-766-5p overexpression, MMP-7 overexpression or miR-766-5p + MMP-7 overexpression wereconstructed. BrdU staining, flow cytometry, and transwell assay were used to assay the cell proliferation, apoptosis, and invasion. The expression levels of related proteins were detected by Westernblotting. Results MiR-766-5p could inhibit the expression of MMP-7. Overexpression of miR-766-5p could inhibit the expression of Ki67, proliferating cell nuclear antigen (PCNA), Wnt1 and β-catenin, and inhibit the proliferation and invasion of U87 cells. It could also promote the expressionof Bcl-associated X protein (Bax) / B-cell lymphoma / leukemia-2 (Bcl-2), and promote cell apoptosis in U87 cells. Overexpression of MMP-7 could partially reverse the effect of miR-766-5p overexpression on U87 cells proliferation, invasion, and apoptosis. Conclusion MiR-766-5p can inhibit the proliferation and invasion of U87 cells, and promote the apoptosis of U87 cells by inhibiting the expression of MMP-7.