MEF2A-mediated lncRNA HCP5 Inhibits Gastric Cancer Progression via MiR-106b-5p/p21 Axis.
MEF2A-mediated lncRNA HCP5 Inhibits Gastric Cancer Progression via MiR-106b-5p/p21 Axis.
复制标题
MEF2A 介导的 lncRNA HCP5 通过 MiR-106b-5p/p21 轴抑制胃癌进展。
DOI：
10.7150/ijbs.55020
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发表时间：
2021
影响因子：
9.2
通讯作者：
Qiu Z
中科院分区：
文献类型：
--
作者：
Chen W;Zhang K;Yang Y;Guo Z;Wang X;Teng B;Zhao Q;Huang C;Qiu Z
背景：长非编码RNA(Long Non-Coding RNAs，LncRNAs)被认为与多种肿瘤的发生发展有关，包括胃癌。我们研究的目的是探讨HCP5在GC中的特征。方法：采用实时定量聚合酶链式反应(qRT-PCR)检测62例配对的胃癌组织和相应的癌旁组织中HCP5的表达。通过体外和体内功能测定，验证了HCP5改变后的生物学效应。染色质免疫沉淀分析(ChIP)证实心肌细胞增强因子2A(MEF2A)可与HCP5启动子区域结合，从而诱导HCP5表达。通过生物信息学预测和荧光素酶报告基因分析miR-106b-5p与HCP5和p21的潜在结合。结果：胃癌组织中HCP5表达明显下调。胃癌患者HCP5表达水平与肿瘤大小和总生存期呈负相关。HCP5缺失对GC细胞的增殖、迁移和侵袭有促进作用。一致地，过度表达HCP5产生了相反的效果。此外，我们还证明了MEF2A可以与HCP5的启动子区域结合，从而诱导HCP5转录。荧光素酶报告分析表明，HCP5可与miR-106b-5p竞争内源RNA(CerNA)，上调胃癌细胞中p21的表达。结论：MEF2A介导的HCP5可通过miR-106b-5p/p21轴在胃癌发生发展过程中发挥抗肿瘤作用，为胃癌的治疗提供了新的靶点。
Background: Long non-coding RNAs (lncRNAs) are deemed to be relevant to the tumorigenesis and development of a variety of tumors, containing gastric cancer (GC). The purpose of our investigations is to explore the character of HCP5 in GC. Methods: HCP5 expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR) in 62 matched GC tissues and corresponding para-carcinoma tissues. In vitro and in vivo functional assays were subjected to verify the biological effects of HCP5 after alteration of HCP5. Chromatin immunoprecipitation assay (CHIP) assays were conducted to confirm that myocyte enhancer factor 2A (MEF2A) could bind to HCP5 promoter regions and thereby induce HCP5 expression. Analysis of the latent binding of miR-106b-5p to HCP5 and p21 was made by bioinformatics prediction and luciferase reporter assays. Results: Significant downregulation of HCP5 was detected in GC tissues. Negative correlation was determined between HCP5 expression level and tumor size and overall survival in GC patients. HCP5 depletion had a facilitating impact on proliferation, migration and invasion of GC cells. Consistently, overexpression of HCP5 came into an opposite effect. Moreover, we demonstrated that MEF2A could combine with the promoter region of HCP5 and thereby induce HCP5 transcription. Luciferase reporter assays revealed that HCP5 could compete with miR-106b-5p as a competing endogenous RNA (ceRNA) and upregulated p21 expression in GC. Conclusions: MEF2A-mediated HCP5 could exert an anti-tumor effect among the development of GC via miR-106b-5p/p21 axis, which provides a novel target for GC therapy.
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影响因子：
28.2
作者：
Karreth FA;Pandolfi PP
通讯作者：
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64.5
作者：
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影响因子：
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影响因子：
16.6
作者：
Tang, Jiayin;Yan, Tingting;Fang, Jing-Yuan
通讯作者：
Fang, Jing-Yuan