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微环境在胃癌发病过程中发挥重要作用。了解胃粘膜早期癌变的分子机制,对防治胃癌具有十分重要的意义。为了解胃粘膜非典型增生过程中,微环境中蛋白质的相互作用及调节机制,采用激光捕获显微切割(laser capture microdissection,LCM)技术,纯化正常胃粘膜组织(normal gastric mucosa tissue,NGM)和胃粘膜非典型增生(gastric mucosal atypical hyperplasia,GMAH)间质,通过同位素标记定量蛋白质组学技术分析,鉴定NGM和GMAH间质的差异表达蛋白质。利用生物信息学软件,分析NGM和GMAH间质差异表达蛋白质的相互作用及其联系。共鉴定出165个GMAH间质差异表达蛋白质,其中GMAH组织中表达上调者99个,下调者66个。它们涉及一些与肿瘤相关的信号通路,如p53信号通路、MAPK信号通路、细胞周期与凋亡等信号通路,且与细胞生长、增殖、凋亡和体液免疫应答等生物学过程有关。这些差异表达蛋白质,在STRING网络中呈现相互作用,两两间相互联系。本文的研究提示,胃粘膜非典型增生微环境中存在S100A6和SOD3等蛋白质间的相互作用,它们通过影响p53信号通路、MAPK信号通路、细胞周期与凋亡等信号通路,在胃癌发病过程中发挥作用。
Microenvironment plays an important role in the pathogenesis of gastric cancer. To understand the molecular mechanism of gastric cancer early cancer, prevention and treatment of gastric cancer has very important significance. In order to understand the interaction and regulation mechanism of proteins in the microenvironment during the process of gastric mucosal atypical hyperplasia, normal gastric mucosa tissue (NGM) was purified by laser capture microdissection (LCM) Gastric mucosal atypical hyperplasia (GMAH) interstitial tissue was identified by isotope labeling quantitative proteomics techniques to identify differentially expressed proteins between NGM and GMAH stroma. Bioinformatics software was used to analyze the interactions and associations of differentially expressed proteins between NGM and GMAH. A total of 165 GMAH interstitial differentially expressed proteins were identified, of which 99 were up-regulated in GMAH tissues and 66 were down-regulated. They involve a number of tumor-related signaling pathways, such as p53 signaling pathway, MAPK signaling pathway, cell cycle and apoptosis signaling pathway, and related to biological processes such as cell growth, proliferation, apoptosis and humoral immune response. These differences in the expression of protein, showing interaction in the STRING network, between the two interrelated. The present study suggests that the interaction between S100A6 and SOD3 in the gastric mucosal atypical hyperplasia microenvironment suggests that they exert their roles in the pathogenesis of gastric cancer by affecting the signaling pathways such as p53, MAPK, cell cycle and apoptosis effect.