Mel-18在子宫内膜癌中的表达及临床意义

Expression and significance of Mel-18 in endometrial cancer

目的:探讨黑色素瘤蛋白(Mel-18)在子宫内膜癌(EC)中的表达及其在肿瘤细胞恶性生物学行为中的作用及机制。方法:免疫组化染色法(IHC)和实时荧光定量聚合酶链式反应(RT-qPCR)检测Mel-18在EC组织及正常子宫内膜组织中的表达。小干扰(siRNA)及腺病毒下调或上调Mel-18在EC细胞系中的表达,MTT法检测Mel-18对EC细胞增殖能力的影响;Transwell小室实验检测Mel-18对EC细胞迁移能力的影响;Western blot法检测相关目的蛋白的表达。结果:IHC和RT-qPCR结果显示,Mel-18在EC组织中显著高表达(P<0.05);腺病毒上调Mel-18在EC细胞系中的表达后,细胞的增殖、迁移能力升高,PI3K/Akt/mTOR信号转导通路表达升高;siRNA下调Mel-18表达抑制细胞的增殖、迁移能力,PI3K/Akt/mTOR信号转导通路表达降低。结论:Mel-18在EC中高表达,在EC的发生发展中可能起到促癌基因的作用,可通过活化PI3K/Akt/mTOR信号转导通路促进EC细胞增殖、迁移能力。

Objective: To detect the expression of Melanoma nuclear protein 18( Mel-18) in endometrial cancer( EC) and evaluate the biological effects of Mel-18 on the proliferation and immigration of EC. Methods: Immunohistochemistry( IHC) and reverse transcription c quantitative polymerase chain reaction( RT-qPCR) assays were used to examine the expression of Mel-18 in EC. Adenovirus and small interfering RNA( siRNA) were used to regulate Mel-18 gene levels in cells.MTT were used to detect the cell proliferation ability.Transwell migration assay was used to detect the cell immigration ability.Western blot was used to detect the related proteins expression. Results: Mel-18 mRNA and protein were both highly expressed in EC( P<0.05).Up-regulation of Mel-18 was significantly promoted the cell proliferation and migration capacity.Loss of Mel-18 was inhibited the cell proliferation and migration ability.We also explored the potential mechanism of Mel-18 in EC cell lines.Overexpression of Mel-18 activated the PI3K/Akt/mT OR pathway,the expressions of PI3K p85α,p-Akt,p-mTOR proteins were significantly increased.Loss of Mel-18 inactivated the PI3K/Akt/mT OR pathway. Conclusion:Mel-18 was highly expressed in EC and promoted cell proliferation and migration via PI3K/Akt/mT OR pathway.