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微小RNA-454-3p对子宫内膜癌细胞生物学行为的影响

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目的 研究微小RNA-454-3p(miR-454-3p)对子宫内膜癌(EC)细胞增殖、侵袭、迁移能力的影响及其机制.方法 用miTED数据库分析miR-454-3p在各组织中的表达水平,用starBase数据库分析EC患者中高表达miR-454-3p组和低表达miR-454-3p组的生存率.用Targetscan预测miR-454-3p的下游靶基因.用Kaplan-Meier Plotter数据库分析EC患者中高表达检测磷酸酯酶与张力蛋白同源物(PTEN)组(高队列的平均表达水平为2 412.45)和低表达PTEN组(低队列的平均表达水平为733.15)的生存率.将Ishikawa细胞分为NC-mimics 组(转染 NC-mimics)、mimics 组(转染 miR-454-3p mimics)、NC-inhibitor组(转染 NC-inhibitor)、inhibitor 组(转染 miR-454-3p inhibitor).用细胞计数试剂盒-8(CCK-8)实验检测细胞的增殖能力,用Transwell和划痕实验分别评估细胞侵袭和迁移能力,用实时定量聚合酶链反应(qRT-PCR)检测PTEN RNA的表达水平.结果 EC患者肿瘤组织与正常组织相比,miR-454-3p的表达水平增高(1.57vs3.26,P<0.05),且低表达miR-454-3p组的生存率显著高于高表达miR-454-3p组(0.74 vs 0.42,P<0.05).NC-mimics组、mimics组、NC-inhibitor组、inhibitor组细胞增殖能力分别为3.73±0.02、5.40±0.02、2.06±0.05 和 1.95±0.05,侵袭细胞数分别为(116±17)、(154±19)、(855±165)和(447±44)个,迁移细胞数分别为(116±8)、(154±27)、(1518±50)和(1 132±175)个,划痕愈合率分别为(20.00±8.00)%、(39.00±2.00)%、(84.00±1.00)%和(52.00±1.00)%,PTEN mRNA表达水平分别为 1.16±0.03、0.94±0.02、0.85±0.14 和 1.22±0.07.mimics组的上述指标与NC-mimics组相比,inhibitor组的上述指标与NC-inhibitor组相比,在统计学上差异均有统计学意义(均P<0.05).EC患者肿瘤组织中PTEN的表达水平显著降低(33.45 vs 17.17,P<0.05),且低表达PTEN组患者生存率显著高于高表达PTEN组(41%vs 93%,P<0.05).结论 miR-454-3p可能通过负调控PTEN的表达促进EC细胞的增殖、侵袭和迁移能力.
Effect of microRNA-454-3p on biological behavior of endometrial cancer cells
Objective To investigate the effect of microRNA-454-3p(miR-454-3p)on the proliferation,invasion,and migration ability of endometrial cancer(EC)cells and its mechanism.Methods Analyze the expression levels of miR-454-3p in various tissues using the miTED database.Analyze the survival rates of high expression miR-454-3p and low expression miR-454-3p groups in EC patients using the starBase database.Use Targetscan to predict downstream target genes of miR-454-3p.Use the Kaplan Meier Plotter database to analyze the survival rates of the high expression detection of phosphatase and tensin homolog(PTEN)group(average expression level in the high cohort:2 412.45)and the low expression of PTEN(average expression level in the low cohort:733.15)in EC patients.Ishikawa cells were divided into NC-mimics group(transfected with NC-mimics),mimics group(transfected with miR-454-3p mimics),NC-inhibitor group(transfected with NC-inhibitor),and inhibitor group(transfected with miR-454-3p inhibitor).Detect the proliferation ability of cells using cell counting kit-8(CCK-8)assay;evaluate cell invasion and migration abilities using Transwell and scratch experiments,respectively;detection of PTEN RNA expression levels using real-time quantitative polymerase chain reaction(qRT-PCR).Results Compared with normal tissue,the expression level of miR-454-3p in tumor tissue of EC patients increased(1.57 vs 3.26,P<0.05),and the survival rate of EC patients with low expression of miR-454-3p increased(0.74 vs 0.42,P<0.05).The cell proliferation ability of the NC mimics group,mimics group,NC inhibitor group and inhibitor group were 3.73±0.02,5.40±0.02,2.06±0.05 and 1.95±0.05;the number of invading cells were 116±17,154±19,855±165 and 447±44;the number of migrating cells were 116±8,154±27,1 518±50 and 1 132±175;the scratch healing rates were(20.00±8.00)%、(39.00±2.00)%、(84.00±1.00)%and(52.00±1.00)%;the expression levels of PTEN mRNA were 1.16±0.03,0.94±0.02,0.85±0.14 and 1.22±0.07,respectively.The differences in the above indicators between the mimics group and the NC mimics group,as well as between the inhibitor group and the NC inhibitor group,were statistically significant(all P<0.05).The expression level of PTEN in tumor tissue of EC patients decreased(33.45 vs 17.17,P<0.05),and the survival rate of EC patients with low expression of PTEN increased(41%vs 93%,P<0.05).Conclusion miR-454-3p may promote the proliferation,invasion,and migration of EC cells by negatively regulating the expression of PTEN.

microRNA-454-3pendometrial cancerproliferationinvasionmigration

潘紫妍、陈雨婷、魏茜茜、王婷、刘杰、胡晨煜、张婷

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石河子大学医学院生物化学教研室/新疆地方与民族高发病教育部重点实验室,新疆维吾尔自治区石河子 832002

微小RNA-454-3p 子宫内膜癌 增殖 侵袭 迁移

国家自然科学基金地区基金资助项目石河子大学校级基金资助项目石河子大学校级基金资助项目

81960152KX01880307KX018904/0305

2024

中国临床药理学杂志
中国药学会

中国临床药理学杂志

CSTPCD北大核心
影响因子:1.91
ISSN:1001-6821
年,卷(期):2024.40(17)