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目的:探讨mi R-150-5p在肝细胞癌(HCC)细胞迁移与侵袭中的作用及其调控机制。方法:用荧光定量PCR测定mi R-150-5p在正常肝细胞系L02及HCC细胞系Hep G2中的表达;将Hep G2细胞分成两组,分别转染mi R-150-5p(mi R-150-5p组)与随机序列(对照组),转染后,分别用细胞划痕实验、Transwell小室基质渗透实验检测细胞的迁移和侵袭能力,用Western blot检测细胞基质金属蛋白酶2(MMP2)和基质金属蛋白酶9(MMP9)的蛋白表达。结果:mi R-150-5p的表达量在Hep G2细胞系中明显降低,为L02细胞系的0.26倍(P<0.01)。转染后,mi R-150-5p组的mi R-150-5p水平明显升高,为对照组的9.53倍(P<0.001);mi R-150-5p组的细胞划痕愈合率明显低于对照组(54.63%vs.87.51%,P<0.01),细胞侵袭数明显少于对照组(138个vs.452个,P<0.01);MMP2与MMP9蛋白表达量均明显低于对照组(0.78 vs.1.75;0.82 vs.1.85,均P<0.05)。结论:mi R-150-5p在HCC细胞中表达降低,升高mi R-150-5p的表达可抑制HCC细胞的迁移和侵袭,机制可能与其下调MMP2和MMP9表达有关。
Objective: To investigate the role of mi R-150-5p in the migration and invasion of hepatocellular carcinoma (HCC) cells and its regulatory mechanism. Methods: The expression of mi R-150-5p in normal liver cell line L02 and HCC cell line Hep G2 was detected by real-time PCR. The Hep G2 cells were divided into two groups and transfected with mi R-150-5p (mi R- 150-5p group) and random sequence (control group). After transfection, cell migration and invasion were evaluated by cell scratch assay and Transwell chamber infiltration assay respectively. The levels of matrix metalloproteinase 2 (MMP2) and Matrix metalloproteinase 9 (MMP9) protein expression. Results: The expression of mi R-150-5p was significantly decreased in Hep G2 cell line, which was 0.26 times of that in L02 cell line (P <0.01). After transfection, the mi R-150-5p level in mi R-150-5p group was significantly increased 9.55-fold (P <0.001) compared with the control group; the wound healing rate in mi R-150-5p group was significantly lower In the control group (54.63% vs.87.51%, P <0.01), the number of cell invasion was significantly less than that in the control group (138 vs.452, P <0.01), and the protein expressions of MMP2 and MMP9 were significantly lower than those in the control group 0.78 vs.1.75; 0.82 vs.1.85, all P <0.05). Conclusions: mi R-150-5p expression is decreased in HCC cells. Increasing mi R-150-5p expression may inhibit the migration and invasion of HCC cells, which may be related to its down-regulation of MMP2 and MMP9 expression.