目的:观察微小核糖核酸-134-5p （miR-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lipo-fectamine 2000将miR-134-5p mimics转染至宫颈癌Hela和SiHa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；qRT-PCR检测宫颈癌组织和细胞miR-134-5p mRNA表达以及宫颈癌细胞EGFR mRNA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miR-134-5p mRNA表达显著低于癌旁组织（P<0.01）。和转染 miR-NC 的 Hela 和 SiHa 细胞比较，转染 miR-134-5pmimics 的宫颈癌 Hela 和 SiHa 细胞 miR-134-5pmRNA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; SiHa细胞：1.12±0.10 vs 1.42±0.12,均P<0.05）；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) %; SiHa细胞: (30.49±12.04）% vs（5.10±2.86)%,均P<0.05]；EGFR mRNA和EGFR蛋白表达显著下调，其中EGFR mRNA，Hela细胞下调58%（P<0.01），SiHa细胞下调41%（P<0.05）；EGFR下游靶蛋白p-AKT、p-ERK1/2和CyclinD1蛋白及pEGFR蛋白表达显著下调。 结论: miR-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。

Objective: To observe effect of miR-134-5p transfection on proliferation and apoptosis of cervical carci-noma cell and to verify its possible molecular mechanism. Methods: Eight pairs of cervical cancer and para-cancer-ous tissuesfrom the patients with cervical cancer who hospitalized in Center of Oncology, Renmin Hospital, Hubei University of Medicine during May to August 2016 were collected. miR-134-5p mimics were transfected into cervi-cal carcinoma Hela and SiHa cells by lipofectomin 2000. MTT and colony formation assays were used to detect pro-liferation of cells. Flow cytometry (FCM）assay was used to test cell cycles and apoptosis of cells. Expressions of miR-134-5p mRNA in cervical carcinoma tissue and cell, and expression of EGFR mRNA in cervical carcinoma cell were detected by qRT-PCR assay. Expressions of EGFR pathway-related proteins in cervical carcinoma cell were examed by Western blotting assay. Results: Expression of miR-134-5p mRNA in cervical carcinoma tissue was significantly lower than that in para-carcinoma tissue (P<0.01). Comparing with the Hela and SiHa cells that transfected with miR-NC, expressions of miR-134-5p mRNA in the Hela and SiHa cells that transfected with miR-134-5p mimics were obviously increased, proliferation abilities of the cells significantly reduced (at the 5th day of the transfection, Hela cell:1.06 ± 0.13 vs 1.32 ± 0.07; SiHa cell: 1.12 ± 0.10 vs 1.42 ± 0.12, all P<0.05), apoptosis rates of the cells obviously increased (Hela cell: [26.53 ± 13.48]% vs [3.25 ± 1.74]%; SiHa cell: [30.49 ± 12.04]% vs [5.12 ±2.86]%, all P<0.05), number of formed colony decreased, ratio of G0/G1 phase cells increased, ratio of the cells in Sand G2/M phase decreased, apoptosis rate of the cells enhanced (all P<0.05), expressions of EGFR mRNA and EG-FR protein in the cells were remarkably down-regulated, among which EGFR mRNA in the the Hela cell down 58%(P<0.01) and in the the SiHa cell down 41% (P<0.05), expressions of downstream target protein for EGFR, p-AKT,p-ERK/2 and Cyclin D1, as well as pEGFR proteins were evidently down-regulated. Conclusion: miR-134-5p couldsignificantly inhibit proliferation of the cervical carcinoma cells and promote their apoptosis, of which possible mo-lecular mechanism might be inhibit activation of EGFR pathway through inhibiting expression of EGFR gene.

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)