TRAF4调控人结直肠癌细胞增殖的机制研究  

The Mechanism of TRAF4 Regulating Proliferation in Human Colon Cancer Cells

作　　者：李伟[1] 罗霞[2,3] 马小倩 

机构地区：[1]中南大学湘雅三医院细胞移植与基因治疗中心,湖南长沙410013 [2]湖南省肿瘤医院 [3]中南大学湘雅医学院附属肿瘤医院中心实验室,湖南长沙410013

出　　处：《激光生物学报》2015年第3期257-262,共6页Acta Laser Biology Sinica

基　　金：国家自然科学基金(81401548;81201171)

摘　　要：目的:研究TRAF4影响结直肠癌细胞增殖的分子机制。方法:MTS和软琼脂集落形成实验检测基因沉默TRAF4后对结直肠癌细胞生长及相关信号通路的影响,检测TRAF4表达下调后结直肠癌细胞的糖酵解变化及己糖激酶II的表达和结直肠细胞对5-Fu的敏感性。结果:基因沉默TRAF4抑制结直肠癌细胞的停泊依赖和停泊非依赖增殖,抑制EGF诱导的Akt活化,下调结直肠癌细胞糖酵解,抑制己糖激酶II的表达,增加结直肠癌细胞对5-Fu的敏感性。结论:TRAF4通过调控糖代谢影响结直肠癌细胞增殖。Objective： To investigate the mechanism of TRAF4 mediated colon cancer cells proliferation. Methods：Colon cancer cells proliferation were tested by MTS and soft agar assayin sh-Mock and sh-TRAF4 stable cell lines. Western blot was conducted to detect the signaling transduction and the expression of Hexokinase II. Then the levels of glycolysis were assessed via measurement of glucose consumption and lactate production,respectively. The sensitivity of these stable cells to 5-Fu was detected by Western blotting. Results： Knockdown TRAF4 attenuates human colon cancer cells anchorage-dependent and-independent growth,TRAF4 knocking down inhibits EGF-induced Akt activation,as well as glycolysis and Hexokinase II expression. Moreover,knockdown TRAF4 increases the sensitivity of colon cancer cells to5-Fu treatment. Conclusion： TRAF4 affects human colon cancer cells proliferation via glycolysis regulation.

关 键 词：结直肠癌 TRAF4 AKT 己糖激酶Ⅱ 糖酵解 

分 类 号：R737.9[医药卫生—肿瘤]