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The mechanism of miR-143 inducing apoptosis of liver carcinoma cells through regulation of the NF-κB pathway

机译:miR-143通过调节NF-κB途径诱导肝癌细胞凋亡的机制

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摘要

Primary hepatic carcinoma is a common malignant tumor with poor treatment efficacy. The effect and mechanism of miR-143 in apoptosis of liver carcinoma cells were investigated in the present study. In vitro transfection of liver carcinoma SMMC-7721 cells was performed using artificially synthesized miR-143 mimics. The proliferation of liver carcinoma cells that were treated was detected by MTT assay. Liver carcinoma cells were then stained using the Annexin V-FITC/PI method, and the apoptosis of stained liver carcinoma cells was measured using a flow cytometer. The relative mRNA expression of NF-κB p65 in the intervention and control groups was assayed using reverse transcription-quantitative polymerase chain reaction, and the protein expression of NF-κB p65 was detected using western blot analysis. The results showed that, in the intervention group, the proliferation rate of cells transfected using miR-143 mimics was significantly lower than that in the control group, the number of apoptotic SMMC-7721 cells in the intervention group increased, and the protein expression of NF-κB p65 was decreased. Thus, miR-143 may downregulate the protein expression of NF-κB p65, thereby triggering the NF-κB signaling transduction pathway inducing apoptosis of liver carcinoma cells.
机译:原发性肝癌是一种常见的恶性肿瘤,治疗效果较差。研究了miR-143在肝癌细胞凋亡中的作用及其机制。使用人工合成的miR-143模拟物进行肝癌SMMC-7721细胞的体外转染。通过MTT分析检测所治疗的肝癌细胞的增殖。然后,使用膜联蛋白V-FITC / PI方法对肝癌细胞进行染色,并使用流式细胞仪测量染色的肝癌细胞的凋亡。采用逆转录定量聚合酶链反应法检测干预组和对照组中NF-κBp65的相对mRNA表达,采用western blot分析检测NF-κBp65的蛋白表达。结果表明,干预组miR-143模拟物转染细胞的增殖率明显低于对照组,干预组凋亡SMMC-7721细胞数量增加,蛋白表达增加。 NF-κBp65降低。因此,miR-143可能下调NF-κBp65的蛋白表达,从而触发NF-κB信号转导途径诱导肝癌细胞凋亡。

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