miR-134-5p对宫颈癌细胞增殖和凋亡的影响及其分子机制

发布时间：2018-05-29 10:52

本文选题：微小核糖核酸--p + 宫颈癌　；参考：《中国肿瘤生物治疗杂志》2017年07期

【摘要】：目的:观察微小核糖核酸-134-5p(mi R-134-5p)转染对宫颈癌细胞增殖和凋亡的影响,验证其可能的分子机制。方法:收集湖北医药学院附属人民医院肿瘤中心2016年5月至8月收治的8名宫颈癌患者肿瘤组织和相应癌旁组织。利用lipofectamine 2000将mi R-134-5p mimics转染至宫颈癌Hela和Si Ha细胞。采用MTT法和集落形成实验检测细胞增殖活性;流式细胞术(FCM)检测细胞周期和细胞凋亡;q RT-PCR检测宫颈癌组织和细胞mi R-134-5p m RNA表达以及宫颈癌细胞EGFR m RNA表达;Western blotting检测宫颈癌细胞EGFR信号通路相关蛋白的表达。结果:宫颈癌组织mi R-134-5p m RNA表达显著低于癌旁组织(P0.01)。和转染mi R-NC的Hela和Si Ha细胞比较,转染mi R-134-5pmimics的宫颈癌Hela和Si Ha细胞mi R-134-5p m RNA表达显著升高;细胞增殖能力显著降低(转染第5天,Hela细胞:1.06±0.13 vs 1.32±0.07;Si Ha细胞:1.12±0.10 vs 1.42±0.12,均P0.05);形成的集落数减少;G0/G1期细胞比例显著上升,S期和G2/M期细胞比例显著下降;细胞凋亡率显著增加[Hela细胞:(26.53±13.48)%vs(3.25±1.74)%;Si Ha细胞:(30.49±12.04)%vs(5.10±2.86)%,均P0.05];EGFR m RNA和EGFR蛋白表达显著下调,其中EGFR m RNA,Hela细胞下调58%(P0.01),Si Ha细胞下调41%(P0.05);EGFR下游靶蛋白p-AKT、p-ERK1/2和Cyclin D1蛋白及p EGFR蛋白表达显著下调。结论:mi R-134-5p可显著抑制宫颈癌细胞增殖并促进细胞凋亡,其可能的分子机制是通过抑制EGFR基因的表达,抑制EGFR通路的活化。
[Abstract]:Aim: to investigate the effect of RNC-134-5pmmi R-134-5p) transfection on the proliferation and apoptosis of cervical cancer cells, and to verify its possible molecular mechanism. Methods: the tumor tissues and adjacent tissues of 8 patients with cervical cancer were collected from the Cancer Center of the people's Hospital affiliated to Hubei Medical College from May to August 2016. Mi R-134-5p mimics was transfected into cervical cancer Hela and SIHA cells by lipofectamine 2000. Cell proliferation activity was detected by MTT assay and colony forming assay. Flow cytometry (FCM) was used to detect the expression of mi R-134-5p m RNA in cervical carcinoma tissues and cells, and the expression of EGFR signal pathway related protein in cervical cancer cells by EGFR m RNA blotting. Results: the expression of mi R-134-5p m RNA in cervical carcinoma was significantly lower than that in paracancerous tissue (P 0.01). Compared with Hela and SIHA cells transfected with mi R-NC, the expression of mi R-134-5p m RNA in Hela and SIHA cells transfected with mi R-134-5pmimics was significantly increased. On the 5th day after transfection, the proliferation of Hela cells was significantly decreased (1.06 卤0.13 vs 1.32 卤0.07Si Ha: 1.12 卤0.10 vs 1.42 卤0.12, all P 0.05), and the number of colony formation decreased significantly in G _ 0 / G _ 1 phase and G _ 2 / M phase. The expression of EGFR-m RNA and EGFR protein were significantly down-regulated in Hela cells. EGFR m RNA-Hela cells down-regulated the down-regulation of the downstream target proteins of 41P0.05EGFR, p-AKTnp-ERK1and Cyclin D1 protein and pEGFR protein in Hela cells (P < 0.05). The apoptosis rate was significantly increased in Hela cells (P < 0.01 卤1.74), and the expression of EGFR-m RNA and EGFR protein was significantly down-regulated in Hela cell line (P0.05EGFR downstream target protein p-AKTFP-ER12 and Cyclin D1 protein and p EGFR protein). The expression of p-AKTP-ERK1.2 and Cyclin D1 protein and p EGFR protein were down-regulated by EGFR m RNA-Hela cells. Conclusion: the cell proliferation and apoptosis of cervical cancer cells were significantly inhibited by 1: mi R-134-5p. The possible molecular mechanism was to inhibit the activation of EGFR pathway by inhibiting the expression of EGFR gene.
【作者单位】：湖北医药学院附属人民医院肿瘤中心;湖北医药学院附属人民医院中药药理实验室;
【基金】：湖北省教育厅科学技术研究资助项目(No.B2016139) 湖北省高校优秀中青年创新基金资助项目(No.T201510)~~
【分类号】：R737.33

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