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目的:探讨微小RNA（miR）-3142在宫颈癌HeLa细胞增殖、侵袭、凋亡和顺铂耐药中的作用及其机制。方法:将体外培养的HeLa细胞分为空白组、阴性组、miR-3142模拟物（mimics）组和miR-3142抑制剂（inhibitor）组，采用实时荧光定量PCR（qPCR）检测HeLa细胞中miR-3142表达水平，噻唑蓝（MTT）法检测HeLa细胞增殖和顺铂耐药性，Transwell小室检测HeLa细胞侵袭，流式细胞仪检测HeLa细胞凋亡情况，双荧光素酶报告基因实验检测miR-3142与第10号染色体缺失的磷酸酶和张力蛋白同源物基因（PTEN）的靶向关系，免疫印迹法（Western blot）检测HeLa细胞中PTEN蛋白表达情况。结果:miR-3142 mimics组细胞中miR-3142（11.47±2.15）表达水平、细胞增殖率[（127.36±11.08）%、（136.25±11.42）%、（145.75±12.35）%]和穿膜细胞数（108.75±8.06）及顺铂对各组细胞的半抑制浓度（IC50）值[（92.36±2.18）、（88.15±2.65）、（76.40±3.85）、68.58±3.85）μmol/L]均明显高于阴性组[（0.96±0.06）、（96.75±5.15）%、（95.48±7.73）%、（98.06±6.22）%、（49.85±4.35）、（85.27±1.05）、（76.33±1.72）、（49.95±2.05）、（34.52±2.88）]，而细胞凋亡率（2.12±0.23）%、细胞中PTEN（0.14±0.02）蛋白表达水平均明显低于阴性组[（10.65±1.13）%、（0.41±0.03）]（n P<0.05）；miR-3142 inhibitor组细胞中miR-3142（0.12±0.01）表达水平、细胞增殖率[（70.13±4.22）%、（62.50±5.06）%、（45.52±3.26）%]和穿膜细胞数（24.36±1.12）及顺铂对细胞的IC50值[（68.52±0.36）、（54.75±0.68）、（26.63±1.26）、（11.44±1.75）]明显低于阴性组，而细胞凋亡率（19.28±2.38）%、细胞中PTEN（1.06±0.09）蛋白表达水平明显高于阴性组（n P<0.05）。n 结论:miR-3142可促进宫颈癌HeLa细胞增殖、侵袭和顺铂耐药性并抑制其凋亡，其作用机制可能与靶向下调PTEN表达有关。“,”Objective:To investigate the role and mechanism of microRNA (miR) -3142 in the proliferation, invasion, apoptosis and cisplatin resistance of cervical cancer HeLa cells.Methods:HeLa cells cultured in vitro were divided into blank group, negative group, miR-3142 mimics group and miR-3142 inhibitor group, real-time quantitative PCR (qPCR) was used to detect the expression level of miR-3142 in HeLa cells, MTT assay was used to detect the proliferation and cisplatin resistance of HeLa cells, Transwell chamber was used to detect the invasion of HeLa cells, the apoptosis of HeLa cells was detected by flow cytometry, double luciferase reporter gene assay was used to detect the targeting relationship between miR-3142 and gene of phosphate and tension homology deleted on chromosome tenphosphatase and tensin homologous gene (PTEN) , and Western blot was used to detect the protein expression of PTEN in HeLa cells.Results:The expression level of miR-3142 (11.47±2.15) , the cell proliferation rate[ (127.36±11.08) %、(136.25±11.42) %、(145.75±12.35) %], the number of penetrating cells (108.75±8.06) and the half inhibitory concentration (IC50) value of cisplatin[ (92.36±2.18) 、(88.15±2.65) 、(76.40±3.85) 、68.58±3.85) μmol/L] in miR-3142 mimics group were significantly higher than those in negative group[ (0.96±0.06) 、(96.75±5.15) %、(95.48±7.73) %、(98.06±6.22) %、(49.85±4.35) 、(85.27±1.05) 、(76.33±1.72) 、(49.95±2.05) 、(34.52±2.88) ], while the apoptosis rate (2.12±0.23) % and PTEN (0.14±0.02) protein expression level were significantly lower[ (10.65±1.13) %、(0.41±0.03) ] (n P<0.05) ; the expression level of miR-3142 (0.12±0.01) , the cell proliferation rate[ (70.13±4.22) %、(62.50±5.06) %、(45.52±3.26) %], the number of penetrating cells (24.36±1.12) and the half inhibitory concentration (IC50) value of cisplatin[ (68.52±0.36) 、(54.75±0.68) 、(26.63±1.26) 、(11.44±1.75) ] in miR-3142 inhibitor group were significantly lower than those in negative group, while the apoptosis rate (19.28±2.38) % and PTEN (1.06±0.09) protein expression level were significantly higher (n P<0.05) .n Conclusion:MiR-3142 can promote the proliferation, invasion and cisplatin resistance of cervical cancer HeLa cells and inhibit its apoptosis. The mechanism may be related to the targeted down-regulation of PTEN expression.