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胃癌的发生和发展是一个多基因、多因素和多阶段的复杂演变过程,涉及多种癌基因和抑癌基因。胃部肿瘤新生血管的存在不但为肿瘤生长提供营养物质,转运代谢产物,还为肿瘤细胞的浸润及转移提供了通道。Maspin、VEGF和iNOS与肿瘤血管的生成密切相关。Maspin通过增加肿瘤细胞同质黏附,防止肿瘤细胞从原病灶脱落,抑制血管生成,诱导肿瘤细胞凋亡而抑制胃癌的发生发展。iNOS通过细胞增殖/凋亡失衡,刺激胃癌新生血管形成参与胃癌的发生。VEGF以自分泌及旁分泌形式刺激胃癌细胞的有丝分裂,诱导胃癌血管形成。Maspin在胃癌组织中的低表达和iNOS、VEGF在胃癌组织中的高表达在胃癌的发生、发展和浸润转移过程中起重要作用。
The occurrence and development of gastric cancer is a multi-gene, multi-factor and multi-stage complex evolution involving multiple oncogenes and tumor suppressor genes. The presence of neovascularization in the stomach tumor not only provides nutrients for tumor growth, translocates metabolites, but also provides a channel for tumor cell infiltration and metastasis. Maspin, VEGF and iNOS are closely related to tumor angiogenesis. Maspin can inhibit the occurrence and development of gastric cancer by increasing the homogeneous adhesion of tumor cells, preventing tumor cells from shedding from the original lesion, inhibiting angiogenesis and inducing tumor cell apoptosis. iNOS, through imbalance of cell proliferation / apoptosis, stimulates the formation of gastric neovascularization in gastric carcinogenesis. VEGF stimulates gastric cancer cell mitosis in an autocrine and paracrine manner, inducing angiogenesis in gastric cancer. The low expression of Maspin in gastric cancer and the high expression of iNOS and VEGF in gastric cancer play an important role in the occurrence, development and invasion and metastasis of gastric cancer.