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作 者:吴小琴[1,2] 曾志荣[2] 许丽霞[2] 曹清华[3] 陈斌[2] 陈旻湖[2] 胡品津[2]
机构地区:[1]广州医科大学附属第二医院消化科,510260 [2]中山大学附属第一医院消化科 [3]中山大学附属第一医院病理科
出 处:《胃肠病学》2014年第2期70-73,共4页Chinese Journal of Gastroenterology
基 金:国家自然科学基金(81201931);广东省自然科学基金(10151008901000223);广州医科大学博士启动项目(2010C06)资助
摘 要:背景:白细胞介素-17A(IL-17A)在炎症反应中发挥重要作用。既往研究发现IL-17A基因多态性与某些亚型胃癌的发生风险增加有关。目的:探讨IL-17A在胃癌中的表达及其对胃癌细胞增殖、凋亡的影响。方法:以免疫组化法和RT-PCR法分别检测胃癌组织、相应癌旁非癌组织以及胃癌细胞株的IL-17A表达。以不同浓度重组人IL-17A处理胃癌细胞株SGC7901,以MTT法检测细胞增殖,以流式细胞术检测细胞凋亡,以real-time RT-PCR检测细胞中的IL-6、基质金属蛋白酶-13(MMP-13)mRNA表达。结果:胃癌组织中IL-17A阳性细胞数较相应癌旁非癌组织显著增多(P<0.05),且主要表达于炎性细胞和血管内皮细胞,在胃癌细胞株中无表达。重组人IL-17A可刺激SGC7901细胞增殖,抑制H_2O_2诱导的细胞凋亡,并上调其IL-6、MMP-13 mRNA表达。结论:IL-17A可直接或通过诱导炎症信号通路分子间接促进胃癌进展。Background:Interleukin-17A (IL-17A) plays a critical role in inflammation.Previous study has shown that IL-17A gene polymorphism is associated with the increased risks of some subtypes of gastric cancer.Aims:To investigate the expression of IL-17A in gastric cancer and its effect on cancer cell proliferation and apoptosis.Methods:Expression of IL-17A in gastric cancer tissue,para-cancer noncancerous tissue and several gastric cancer cell lines was determined by immunohistochemistry and RT-PCR.Gastric cancer cell line SGC7901 was treated with different concentrations of recombinant human IL-17A; cell proliferation was measured by MTT assay,cell apoptosis was assessed by flow cytometry,and expressions of IL-6 and matrix metalloproteinase-13 (MMP-13) mRNA were determined by real-time RT-PCR in SGC7901 cells.Results:Expression of IL-17A in gastric cancer tissue was significantly increased when compared with that in para-cancer noncancerous tissue (P < 0.05),and it was mainly expressed in inflammatory cells and vascular endothelial cells; IL-17A was not expressed in gastric cancer cell lines.Proliferation of SGC7901 cells was induced and H2 O2-induced cell apoptosis was inhibited by recombinant human IL-17A.Expressions of IL-6 and MMP-13 mRNA were significantly upregulated in SGC7901 cells treated by recombinant human IL-17A.Conclusions:IL-17A may enhance the progression of gastric cancer directly or indirectly through inducing inflammatory signal pathway related molecules.
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