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长链非编码 RNA MALAT1 通过海绵吸附 miR-363-3p 来调节 EZH2 表达,促进结直肠癌的发展。

LncRNA MALAT1 promotes colorectal cancer development by sponging miR-363-3p to regulate EZH2 expression.

机构信息

Department of Anorectal Surgery, The First People's Hospital of Wenling, Zhejiang Province, China.

Department of General Surgery, The First People's Hospital of Wenling, Zhejiang Province, China.

出版信息

J Biol Regul Homeost Agents. 2019 Mar-Apr;33(2):331-343.

PMID:30972996
Abstract

LncRNA MALAT1 is reported to play a potential role in human cancers. Hence, we investigated the effects of MALAT1 on colorectal cancer and , and further validated whether MALAT1 affected colorectal cancer development and EZH2 expression via regulating miR-363-3p. The fresh colorectal cancer tissues, adjacent non-tumor tissues, FHC, LOVO, SW620, CL40 and HCT116 cells were analyzed in this study. MALAT1, miR-363-3p and EZH2 expression levels were assessed using qRT-PCR and Western blot. Cell proliferation, migration and invasion were also measured. Binding effects between MALAT1 and miR-363-3p, or miR-363-3p and EZH2 3'UTR were detected by dual luciferase assay. We observed that MALAT1 was highly expressed in colorectal cancer tissues and cells, and MALAT1 knockdown inhibited cell proliferation as well as expression levels of EZH2 by upregulated miR-363-3p in cell models and . Moreover, miR-363-3p functions as a downstream target of MALAT1, meanwhile EZH2 was a target of miR-363-3p, suggesting MALAT1 might regulate miR-363-3p and/or EZH2 expression. Collectively, we concluded that MALAT1 functioned as a ceRNA to promote colorectal cancer development and EZH2 expression through sponging miR-363-3p and .

摘要

长链非编码 RNA MALAT1 被报道在人类癌症中发挥潜在作用。因此,我们研究了 MALAT1 对结直肠癌的影响,并进一步验证了 MALAT1 是否通过调节 miR-363-3p 影响结直肠癌的发生和 EZH2 表达。本研究分析了新鲜结直肠癌组织、相邻非肿瘤组织、FHC、LOVO、SW620、CL40 和 HCT116 细胞。采用 qRT-PCR 和 Western blot 检测 MALAT1、miR-363-3p 和 EZH2 的表达水平。还测量了细胞增殖、迁移和侵袭。通过双荧光素酶报告基因检测 MALAT1 与 miR-363-3p 或 miR-363-3p 与 EZH2 3'UTR 之间的结合效应。我们观察到 MALAT1 在结直肠癌组织和细胞中高表达,MALAT1 敲低通过上调细胞模型中的 miR-363-3p 抑制细胞增殖以及 EZH2 的表达水平。此外,miR-363-3p 是 MALAT1 的下游靶标,而 EZH2 是 miR-363-3p 的靶标,表明 MALAT1 可能通过海绵吸附 miR-363-3p 调节 MALAT1 和/或 EZH2 的表达。综上所述,我们得出结论,MALAT1 通过海绵吸附 miR-363-3p 促进结直肠癌的发展和 EZH2 的表达。

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