关键词: BVES POPDC1 POPEYE colitis-associated cancer

Mesh : Animals Carcinogenesis / metabolism Cell Adhesion Molecules Humans Membrane Proteins / metabolism Muscle Proteins Neoplasms / metabolism Signal Transduction / physiology Tight Junctions / metabolism

来  源:   DOI:10.1080/21688370.2018.1499843   PDF(Sci-hub)   PDF(Pubmed)

Abstract:
Blood vessel epicardial substance (BVES) is a tight-junction associated protein that was originally discovered from a cDNA screen of the developing heart. Research over the last decade has shown that not only is BVES is expressed in cardiac and skeletal tissue, but BVES is also is expressed throughout the gastrointestinal epithelium. Mice lacking BVES sustain worse intestinal injury and inflammation. Furthermore, BVES is suppressed in gastrointestinal cancers, and mouse modeling has shown that loss of BVES promotes tumor formation. Recent work from multiple laboratories has revealed that BVES can regulate several molecular pathways, including cAMP, WNT, and promoting the degradation of the oncogene, c-Myc. This review will summarize our current understanding of how BVES regulates the intestinal epithelium and discuss how BVES functions at the molecular level to preserve epithelial phenotypes and suppress tumorigenesis.
摘要:
血管心外膜物质(BVES)是一种紧密连接相关的蛋白质,最初是从发育中的心脏的cDNA筛选中发现的。过去十年的研究表明,BVES不仅在心脏和骨骼组织中表达,但BVES也在整个胃肠道上皮中表达。缺乏BVES的小鼠维持更坏的肠损伤和炎症。此外,BVES在胃肠道癌症中被抑制,小鼠模型显示BVES的缺失促进肿瘤形成。多个实验室最近的工作表明,BVES可以调节几种分子途径,包括cAMP,WNT,促进癌基因的降解,c-Myc.这篇综述将总结我们目前对BVES如何调节肠上皮的理解,并讨论BVES如何在分子水平上发挥功能以保留上皮表型和抑制肿瘤发生。
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