Zhang He-Liang, Liu Chong-Yuan, Ma Wei, Huang Lin, Li Chang-Jian, Li Cheng-Song, Zhang Zhi-Wei
Key Laboratory of Cancer Cellular and Molecular Pathology, Cancer Research Institute of Medical College, University of South China, Hengyang, Hunan 421001, P.R. China.
Medical Company, Troops 66028 of People's Liberation Army, Chengde, Hebei 067000, P.R. China.
Oncol Lett. 2018 Aug;16(2):2355-2365. doi: 10.3892/ol.2018.8941. Epub 2018 Jun 11.
In the present study, the interaction of proteins in the microenvironment of gastric mucosal atypical hyperplasia was analyzed. The stromata of normal gastric mucosa (NGM) and gastric mucosal atypical hyperplasia (GMAH) tissues were purified with laser capture microdissection (LCM). The differentially expressed GMAH proteins of the NGM and GMAH tissues were identified by quantitative proteomic techniques with isotope labeling. The cross-talk between differentially expressed proteins in NGM and GMAH tissues was then analyzed by bioinformatics. There were 165 differentially expressed proteins identified from the stromata of NGM and GMAH tissues. Among them, 99 proteins were upregulated and 66 were downregulated in GMAH tissue. The present study demonstrated that these proteins in gastric mucosal atypical hyperplasia were involved in cancer-associated signaling pathways, including the p53, mitogen-activated protein kinase (MAPK), cell cycle and apoptosis signaling pathways, and were involved in cellular growth, cellular proliferation, apoptosis and the humoral immune response. The results of the present study suggest that the 165 differentially expressed proteins, including S100 calcium-binding protein A6 (S100A6) and superoxide dismutase 3 (SOD3) in the microenvironment of gastric mucosal atypical hyperplasia, are involved in the p53, MAPK, cell cycle and apoptosis signaling pathways, and serve a function in the pathogenesis of gastric cancer.
在本研究中,分析了胃黏膜非典型增生微环境中蛋白质的相互作用。采用激光捕获显微切割(LCM)技术纯化正常胃黏膜(NGM)和胃黏膜非典型增生(GMAH)组织的基质。运用同位素标记定量蛋白质组学技术鉴定NGM和GMAH组织中差异表达的GMAH蛋白。随后通过生物信息学分析NGM和GMAH组织中差异表达蛋白之间的相互作用。从NGM和GMAH组织的基质中鉴定出165种差异表达蛋白。其中,GMAH组织中有99种蛋白上调,66种蛋白下调。本研究表明,胃黏膜非典型增生中的这些蛋白参与癌症相关信号通路,包括p53、丝裂原活化蛋白激酶(MAPK)、细胞周期和凋亡信号通路,并参与细胞生长、细胞增殖、凋亡和体液免疫反应。本研究结果提示,胃黏膜非典型增生微环境中的165种差异表达蛋白,包括S100钙结合蛋白A6(S100A6)和超氧化物歧化酶3(SOD3),参与p53、MAPK、细胞周期和凋亡信号通路,并在胃癌发病机制中发挥作用。