胃癌中BTG3表达的临床病理意义及抑瘤作用的机制  

Roles of BTG3 Expression in Gastric Cancer and Mechanism for Its Tumor Suppression Function

作　　者：郑华川[1] 申道福 杨雪峰[1] 勾文峰[1] 赵爽[1] 张文陆[1] 

机构地区：[1]辽宁医学院附属第一医院肿瘤中心辽宁省脑与脊髓损伤重点实验室实验动物中心,辽宁锦州121001

出　　处：《中国医科大学学报》2015年第10期877-882,共6页Journal of China Medical University

基　　金：国家自然科学基金(81172371;81472544);辽宁省教育厅优秀人才计划(LJQ2014093);辽宁省科学技术厅2012年博士启动资助项目(20121095);辽宁医学院2012年博士启动项目(Y2012B018);辽宁医学院校长基金(XZJJ20140201;XZJJ20140203)

摘　　要：目的研究胃癌中BTG3表达的临床病理意义,揭示BTG3对胃癌细胞恶性表型的逆转作用。方法采用联合组织芯片和免疫组化检测胃癌中BTG3表达,胃癌细胞MKN28和MGC803过表达BTG3,分别利用CCK-8、PI染色、碱性磷酸酶活性测定和GFP-LC-3B转染观察细胞增殖、细胞周期、分化和自噬。结果 BTG3过表达可以抑制胃癌细胞增殖、诱导细胞周期S/G2期阻滞、分化和自噬(P<0.05),胃癌组织中BTG3表达下调(P<0.05),BTG3表达与胃癌静脉侵袭和去分化呈正相关(P<0.05)。结论BTG3表达下调参与胃癌发生和演进过程,BTG3过表达可以逆转胃癌恶性表型,可以作为胃癌基因治疗的潜在靶点。Objective To clarify the clinicopathological significance and the reversing effects of BTG3 expression on the aggressive phenotype in gastric cancer. Methods BTG3 expression was detected in gastric cancer tissues by on tissue microarray and immunostaining. BTG3-expressing plasmid was transfected into MKN28 and MGC803 cells,the proliferation,cell cycle,differentiation and autophagy were analyzed by CCK-8,PI staining,alkaline phosphatase activity and GFP-LC-3B transfection,respectively. Results BTG3 overexpression inhibited cell proliferation,induced S/G2 arrest,differentiation and autophagy in both cells（P〈0.05）. BTG3 expression was decreased in gastric cancer in comparison with the adjacent mucosa（P〈0.05）,and positively correlated with venous invasion and dedifferentiation of the cancers（P〈0.05）. Conclusion BTG3 expression contributes to gastric carcinogenesis and subsequent progression. BTG3 overexpression can reverse the aggressive phenotypes,which could be employed as a potential target for gene therapy of gastric cancer.

关 键 词：胃癌 BTG3 肿瘤发生 病理生物学行为 基因治疗 

分 类 号：R731[医药卫生—肿瘤]