TRAF4调控人结直肠癌细胞增殖的机制研究

摘要

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. West-ern blot was conducted to detect the signaling transduction and the expression of Hexokinase II. Then the levels of glycol-ysis 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 to 5-Fu treatment. Conclusion: TRAF4 affects human colon cancer cells proliferation via glycolysis regulation.%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。