咖啡酸苯乙酯对结肠癌细胞JNK-paxillin信号通路的影响

目的:探讨咖啡酸苯乙酯(CAPE)对结肠癌细胞增殖抑制作用及对c-jun氨基酸末端激酶(JNK)信号通路的影响。方法:体外培养人结肠癌细胞株(HT-29),采用MTT法观察不同浓度的CAPE在不同时间段对HT-29细胞生长的抑制率;不同浓度的CAPE处理HT-29细胞24 h后,用Western blot法检测细胞中JNK及paxillin两种蛋白表达量的变化。结果:4个浓度(2.5,5.0,7.5,10.0μg/L)的CAPE均能明显抑制结肠癌细胞HT-29的增殖,且呈现明显的浓度和时间依赖性(均P<0.01);4个浓度的CAPE均能降低JNK和paxillin蛋白表达水平,且呈明显的浓度依赖性(均P<0.01)。结论:CAPE可在体外抑制人结肠癌细胞HT-29的增殖,机制可能与其降低JNK-paxillin信号通路的活性有关。

Influence of caffeic acid phenethyl ester on JNK-Paxillin signaling pathway in colon cancer cell

Objective: To investigate the inhibitory effect of caffeic acid phenethyl ester(CAPE) on human colon cancer HT-29 cells and its influence on the c-Jun N-terminal kinase(JNK) signaling complex. Methods: The human colon cancer HT-29 cells were cultured in vitro,and then the inhibition rate of cell growth was measured by MTT assay after the HT-29 cells were exposed to different concentrations of CAPE over different time periods.Next,the expression levels of JNK and paxillin protein in HT-29 cells were detected by Western blot analysis after 24 h exposure to different concentrations of CAPE. Results: All the 4 concentrations(2.5,5.0,7.5 and 10.0 μg/L) of CAPE inhibited the proliferation of HT-29 cells,which showed a concentration-and time-dependent effect(all P<0.01).All the 4 concentrations of CAPE decreased the expression levels of JNK and paxillin protein,which showed a concentration-dependent effect(all P<0.01). Conclusion: CAPE can inhibit the proliferation of human colon cancer HT-29 cells in vitro,and the mechanism may be related to its reducing the activity of JNK-paxillin signaling pathway.