中国肿瘤临床
中國腫瘤臨床
중국종류림상
CHINESE JOURNAL OF CLINICAL ONCOLOGY
2012年
22期
1726-1729
,共4页
刘省宇%苗智峰%武剑华%由一%徐昊%王振宁%徐惠绵
劉省宇%苗智峰%武劍華%由一%徐昊%王振寧%徐惠綿
류성우%묘지봉%무검화%유일%서호%왕진저%서혜면
胃癌%肿瘤相关巨噬细胞%上皮间质转化%腹膜转移癌
胃癌%腫瘤相關巨噬細胞%上皮間質轉化%腹膜轉移癌
위암%종류상관거서세포%상피간질전화%복막전이암
Gastric cancer%Tumor-associated macrophages%Epithelial-mesenchymal transition%Peritoneal carcinomatosis
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.
目的:研究胃癌細胞對巨噬細胞的誘導作用,分析活化巨噬細胞對間皮細胞的損傷作用及機製.方法:人正常胃腺上皮細胞繫GES-1及人低分化胃癌細胞繫SGC-7901與人單覈巨噬細胞THP-1共培養,誘導後者分化,研究後者對人腹膜間皮細胞HMR-sv5的損傷作用及分子機製.結果:胃癌細胞誘導THP-1形成腫瘤相關巨噬細胞(TAM),M1型巨噬細胞錶麵抗原的錶達顯著下調,而M2錶型的錶麵抗原明顯上調,細胞形態也髮生明顯改變.TAM顯著抑製正常間皮細胞生長,促進間皮細胞凋亡和上皮間質轉化.結論:胃癌細胞誘導巨噬細胞髮生錶型和功能轉化,進而導緻間皮細胞髮生EMT和凋亡,促進形成腹膜轉移癌.
목적:연구위암세포대거서세포적유도작용,분석활화거서세포대간피세포적손상작용급궤제.방법:인정상위선상피세포계GES-1급인저분화위암세포계SGC-7901여인단핵거서세포THP-1공배양,유도후자분화,연구후자대인복막간피세포HMR-sv5적손상작용급분자궤제.결과:위암세포유도THP-1형성종류상관거서세포(TAM),M1형거서세포표면항원적표체현저하조,이M2표형적표면항원명현상조,세포형태야발생명현개변.TAM현저억제정상간피세포생장,촉진간피세포조망화상피간질전화.결론:위암세포유도거서세포발생표형화공능전화,진이도치간피세포발생EMT화조망,촉진형성복막전이암.
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-SV5 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-SV5, 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.