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Abstract：
The underexpression of the long noncoding RNA blood vessel epicardial substance antisense RNA 1 (BVES-AS1) has been shown in colon adenocarcinoma (COAD) patients. However, its role in COAD remains to be explored. This study aimed to investigate the function and potential mechanism of BVES-AS1 in COAD. Colony formation, Cell Counting Kit-8, JC-1 mitochondrial membrane potential assay, wound healing, transwell, and western blot analyses were used to measure cell proliferation, apoptosis, migration, invasion, and epithelial-mesenchymal transition (EMT) in COAD cells. RNA pull-down, luciferase reporter, and RNA binding protein immunoprecipitation assays were used to detect the interaction of BVES-AS1 and downstream genes. BVES-AS1 was expressed at low levels in COAD cells. Overexpressed BVES-AS1 inhibited COAD cell proliferation, migration, invasion, and EMT while elevating cell apoptosis. Mechanistically, BVES-AS1 functioned as a competing endogenous RNA sponging miR-522-3p to regulate the expression of nearby gene blood vessel epicardial substance (BVES). Besides this, BVES-AS1 recruited TATA-box binding protein associated factor 15 (TAF15) to promote BVES messenger RNA stability. Taken together, our study confirmed that BVES-AS1 inhibited COAD progression via interacting with miR-522-3p and TAF15 to regulate BVES expression, which might offer a perspective for COAD treatment.
摘要：
在结肠腺癌（COAD）患者中已显示长链非编码RNA血管心外膜物质反义RNA1（BVES-AS1）的表达不足。然而,它在COAD中的作用还有待探索。本研究旨在探讨BVES-AS1在COAD中的作用及可能的作用机制。殖民地的形成,细胞计数试剂盒-8，JC-1线粒体膜电位测定，伤口愈合，transwell,和蛋白质印迹分析用于测量细胞增殖，凋亡，迁移,入侵,和COAD细胞中的上皮-间质转化（EMT）。RNA下拉，荧光素酶报告基因,和RNA结合蛋白免疫沉淀法检测BVES-AS1与下游基因的相互作用。BVES-AS1在COAD细胞中以低水平表达。过表达BVES-AS1抑制COAD细胞增殖,迁移,入侵,和EMT同时升高细胞凋亡。机械上,BVES-AS1作为形成miR-522-3p的竞争性内源性RNA起作用,以调节附近基因血管心外膜物质(BVES)的表达。除此之外,BVES-AS1招募TATA-box结合蛋白相关因子15（TAF15）以促进BVES信使RNA的稳定性。一起来看,我们的研究证实，BVES-AS1通过与miR-522-3p和TAF15相互作用以调节BVES表达来抑制COAD进展，这可能为COAD治疗提供一个视角。
