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./nMethods: 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./nResults: 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./nConclusions: 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.

中文翻译：

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MEF2A 介导的 lncRNA HCP5 通过 MiR-106b-5p/p21 轴抑制胃癌进展

背景：长链非编码 RNA (lncRNA) 被认为与包括胃癌 (GC) 在内的多种肿瘤的发生和发展有关。我们研究的目的是探索 HCP5 在 GC 中的特征。/n方法：通过定量实时聚合酶链反应 (qRT-PCR) 在 62 个匹配的 GC 组织和相应的癌旁组织中检测 HCP5 表达。体外和体内功能测定用于验证 HCP5 改变后 HCP5 的生物学效应。进行染色质免疫沉淀测定 (CHIP) 测定以确认肌细胞增强因子 2A (MEF2A) 可以与 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检测分析 miR-106b-5p 与 HCP5 和 p21 的潜在结合。/n结果：在 GC 组织中检测到 HCP5 的显着下调。HCP5 表达水平与 GC 患者的肿瘤大小和总生存率之间确定了负相关。HCP5 耗竭对 GC 细胞的增殖、迁移和侵袭具有促进作用。一致地，HCP5 的过度表达会产生相反的效果。此外，我们证明了 MEF2A 可以与 HCP5 的启动子区域结合，从而诱导 HCP5 转录。荧光素酶报告基因检测显示 HCP5 可以与 miR-106b-5p 作为竞争性内源性 RNA (ceRNA) 竞争并上调 GC 中 p21 的表达。/n结论： MEF2A 介导的 HCP5 可以通过以下方式发挥抗肿瘤作用miR-106b-5p/p21 轴，为 GC 治疗提供了新的靶点。