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首页> 外文期刊>Journal of cellular and molecular medicine. >The long non‐coding RNA SNHG1 promotes bladder cancer progression by interacting with miR‐143‐3p and EZH2
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The long non‐coding RNA SNHG1 promotes bladder cancer progression by interacting with miR‐143‐3p and EZH2

机译:长期非编码RNA SnHG1通过与miR-143-3P和EZH2相互作用来促进膀胱癌进展

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The long non-coding RNA (lncRNA) SNHG1 has been shown to be implicated in the progression of multiple human carcinomas. Nevertheless, the biological functions and potential mechanism of SNHG1 in bladder cancer (BC) are uncharacterized. In the present study, SNHG1 was found to be substantially up-regulated in BC tissues and cells and was intimately correlated with the TNM stage, lymphatic invasion, metastasis and recurrence-free survival in BC patients. Down-regulation of SNHG1 dramatically attenuated the proliferation, migration and invasion of BC cells, whereas the ectopic overexpression of SNHG1 had the opposite effects in vitro. The in vivo experimental results also indicated that SNHG1 down-regulation hampered the tumour growth and metastasis of BC cells. Mechanistic investigations revealed that SNHG1 enhances HK2 expression by serving as an endogenous sponge to regulate miR-143-3p in the cytoplasm of BC cells. In the nucleus, SNHG1 could interact with EZH2 and regulate the histone methylation of the CDH1 promoter, altering the biological behaviours of BC cells. Overall, these findings elucidate an oncologic role of SNHG1 in BC and provide a new therapeutic strategy against BC.? 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
机译:已经显示了长的非编码RNA(LNCRNA)SNHG1与多种人癌的进展相关。然而,膀胱癌(BC)中SNHG1的生物功能和潜在机制是无表的。在本研究中,发现SNHG1在BC组织和细胞中基本上调节,并与BC患者的TNM阶段,淋巴侵入,转移和复发存活密切相关。 SNHG1的下调显着减弱了BC细胞的增殖,迁移和侵袭,而SNHG1的异位过度表达在体外具有相反的效果。体内实验结果还表明,SNHG1下调阻碍了BC细胞的肿瘤生长和转移。机械研究表明,通过用作内源海绵来调节BC细胞的细胞质中的miR-143-3p,SNHG1增强HK2表达。在核中,SNHG1可以与EZH 2相互作用并调节CDH1启动子的组甲基化,改变BC细胞的生物学行为。总体而言,这些研究结果阐明了BC中SNHG1的肿瘤作用,并为BC提供了新的治疗策略。 2020作者。细胞和分子医学基础和约翰瓦里&SONS&LTD的蜂窝和分子医学杂志。

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