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作 者:刘省宇[1] 苗智峰[1] 武剑华[1] 由一[1] 徐昊[1] 王振宁[1] 徐惠绵[1]
机构地区:[1]中国医科大学附属第一医院肿瘤外科,沈阳市110001
出 处:《中国肿瘤临床》2012年第22期1726-1729,共4页Chinese Journal of Clinical Oncology
基 金:国家自然科学基金项目(编号:81071956)资助~~
摘 要:目的:研究胃癌细胞对巨噬细胞的诱导作用,分析活化巨噬细胞对间皮细胞的损伤作用及机制。方法:人正常胃腺上皮细胞系GES-1及人低分化胃癌细胞系SGC-7901与人单核巨噬细胞THP-1共培养,诱导后者分化,研究后者对人腹膜间皮细胞HMR-sv5的损伤作用及分子机制。结果:胃癌细胞诱导THP-1形成肿瘤相关巨噬细胞(TAM),M1型巨噬细胞表面抗原的表达显著下调,而M2表型的表面抗原明显上调,细胞形态也发生明显改变。TAM显著抑制正常间皮细胞生长,促进间皮细胞凋亡和上皮间质转化。结论:胃癌细胞诱导巨噬细胞发生表型和功能转化,进而导致间皮细胞发生EMT和凋亡,促进形成腹膜转移癌。Objective:This work aims to determine the effects of the induction of gastric cancer cells on macrophages and the damaging effect of activated peritoneal macrophages on the peritoneal mesothelial cells. Methods:The human macrophage cell line THP- 1 was co-cultured with either the human normal gastric epithelial cell line GES-1 or the poorly differentiated human gastric cancer cell line SGC-7901 . The induction effects of the gastric cells on the THP- 1 cells was then studied. The effects of the activated macrophages on the human peritoneal mesothelial cell line HMR-SV 5 were further studied.Results:The gastric cancer cell line SGC-7901 induced THP- 1 cells to become tumor-associated macrophages (TAM), which had distinctive morphological features. Induction significantly reduced the expression of the M1-type macrophage surface antigens, such as CD80 and CD86 , and significantly increased the expression of the M2-type macrophage surface antigens, such as CD163. The activated macrophages brought about a significant growth inhibition and apoptosis of the mesothelial cell HMR-SV 5, The HMR-SV5 cell also underwent a conspicuous epithelial-mesenchymal transition (EMT). Conclusion:Gastric cancer cells could induce morphological and phenotypic changes in the macrophages, which can in turn cause mesothelial cell damage, apoptosis, and EMT, thus creating a favorable microenvironment for peritoneal carcinomatosis.
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