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首页> 外文期刊>Journal of cellular physiology. >MTSS1 hypermethylation is associated with prostate cancer progression
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MTSS1 hypermethylation is associated with prostate cancer progression

机译：MTSS1甲基化与前列腺癌有关癌症恶化

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This study was conducted to evaluate the influence of DNA methylation of metastasis suppressor 1 [MTSS1) on prostate cancer (PCa) progression. Forty-nine paired PCa tissue samples and normal tissue samples from The Cancer Genome Atlas were analyzed. Methylome analysis, CpG island arrays and Hierarchical clustering were used to analyze methylation profiles of PCa tissues. MTSS1 methylation level was detected by methylation-specific PCR. Relative messenger RNA and the expression level of MTSS1 protein were identified by quantitative real-time PCR (qRT-PCR) and western blot analysis. The migration, invasion, proliferation, and cell cycle were detected separately by wound-healing assay, transwell chamber assay, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetra-zolium bromide assay and flow cytometry. The roles of MTSS1 in PCa progression were demonstrated in vivo by tumor formation assays in nude mice. MTSS1 expression was decreased in PCa tissues in comparison with paired adjacent normal prostate tissues. Compared to the methylation of MTSS1 in normal prostate tissues based on the MethHC website, the MTSS1 in PCa tissues was hypermethylated. The expression of MTSS1 detected by qRT-PCR and western blot analysis was found to be downregulated in PCa cells and tissues. The reduced expression of MTSS1 by small interfering RNA-MTSS1 was recovered by 5-aza-2'-deoxycytidine treatment. Besides, MTSS1 demethylation inhibited migration, invasion, and proliferation of PCa cells, and induced cell cycle to be arrested at G0/G1 phase. Furthermore, it was shown by tumor xenograft assay that MTSS1 inhibited the growth of tumor in vivo. Hypermethylated MTSS1 promoted PCa cells migration, invasion, and proliferation, and suppressed cell cycle arrest at the G0/G1 phase.
机译：这项研究进行了评估的影响的DNA甲基化转移抑制因子1[MTSS1)在前列腺癌(PCa)发展。49 PCa组织样本和正常配对组织样本的癌症基因组图谱分析。和分层聚类分析甲基化的PCa组织。甲基化水平被检测到methylation-specific PCR。和MTSS1蛋白的表达水平被定量实时PCR(存在)和免疫印迹分析。迁移、入侵、增殖和细胞周期被愈合分别检测transwell室试验分析,(3) - 4 5-dimethylthiazol-2-yl 2, 5-diphenyltetra-zolium溴化分析和流式细胞术。在PCa进展MTSS1的角色证明了体内的肿瘤形成化验裸小鼠。组织与相邻正常配对相比前列腺组织。MTSS1在正常前列腺组织的基础上MethHC网站,MTSS1 PCa组织hypermethylated。被发现存在和免疫印迹分析PCa细胞和组织中表达下调。表达MTSS1减少了小干扰恢复了RNA-MTSS1 5-aza-2脱氧胞苷治疗。主成分分析的迁移、入侵和扩散细胞,诱导细胞周期被逮捕G0 / G1期。异种移植试验,MTSS1抑制了增长体内的肿瘤。PCa细胞迁移、入侵和扩散,和抑制细胞周期阻滞于G0 / G1阶段。

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