Psoralidin inhibits proliferation and enhances apoptosis of human esophageal carcinoma cells via NF-κB and PI3K/Akt signaling pathways
Psoralidin inhibits proliferation and enhances apoptosis of human esophageal carcinoma cells via NF-κB and PI3K/Akt signaling pathways
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DOI：
10.3892/ol.2016.4716
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发表时间：
2016-08-01
期刊：
影响因子：
2.9
通讯作者：
Xu, Yanhua
中科院分区：
文献类型：
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作者：
Jin, Zhiliang;Yan, Wei;Xu, Yanhua
食道癌是最常见的胃肠道肿瘤。补骨脂具有抗氧化、抗凋亡、抗炎、抗肿瘤等作用，具有抑制肿瘤形成的作用。本研究旨在探讨补骨脂素对食管癌增殖和生长的影响，并探讨其作用机制。采用四甲基偶氮唑蓝(3-(4，5-dimethylthiazol-2-yl)-2，5-diphenyltetrazolium)比色法观察补骨脂素对细胞增殖的影响。应用Annexin V-异硫氰酸荧光素/碘化丙啶细胞凋亡检测试剂盒和4‘，6-二氨基-2-苯基吲哚染色方法，本研究证实补骨脂素显著促进人食道癌Eca9706细胞的凋亡。采用半胱氨酸天冬氨酸氨基转移酶-3(caspase-3)比色试剂盒检测半胱氨酸天冬氨酸氨基转移酶-3(caspase-3)活性，用核因子-kappaB(NF-kappa B)酶联免疫吸附分析试剂盒检测核因子-kappaB活性，用免疫印迹法检测蛋白磷脂酰肌醇3-激酶(PI3K)/Akt的表达。用PI3K激动剂处理Eca9706细胞，以探讨补骨脂素的作用机制。补骨脂素能抑制Eca9706细胞增殖，促进细胞凋亡，且呈剂量依赖关系。补骨脂素还能抑制Eca9706细胞的caspase-3活性，且呈剂量依赖关系。此外，补骨脂素还可抑制Eca9706细胞中核因子-kappaB的活性，降低PI3K和Akt蛋白的表达。值得注意的是，PI3K激动剂能够逆转补骨脂素对Eca9706细胞的作用。本研究结果表明，补骨脂素可通过核因子-kappaB和PI3K/A kt信号通路抑制人食道癌细胞增殖，促进细胞凋亡。
Esophageal cancer is the most common gastrointestinal cancer. Psoralidin exhibits antioxidant, anti-apoptotic, anti-inflammatory and antitumor effects, which result in the inhibition of cancer formation. The present study aimed to investigate the effect of psoralidin on esophageal carcinoma proliferation and growth, and to elucidate its underlying mechanism of action. The effect of psoralidin on cell proliferation was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Using an annexin V-fluorescein isothiocyanate/propidium iodide apoptosis detection kit and 4',6-diamidino-2-phenylindole staining assay, the present study demonstrated that psoralidin significantly enhanced apoptosis of human esophageal carcinoma Eca9706 cells. In addition, caspase-3 activity was analyzed with a caspase-3 colorimetric assay kit, while nuclear factor (NF)-kappa B activity and protein phosphatidylinositol 3-ki nase (PI3K)/Akt expression were measured with an NF-kappa B enzyme-linked immunosorbent assay kit and western blot analysis, respectively. Eca9706 cells were treated with a PI3K agonist in order to investigate the mechanism of action of psoralidin. It was observed that psoralidin was able to decrease the proliferation and promote the cellular apoptosis of Eca9706 cells in a dose-dependent manner. Furthermore, psoralidin was also able to inhibit the caspase-3 activity of Eca9706 cells in a dose-dependent manner. In addition, psoralidin inhibited NF-kappa B activity and reduced PI3K and Akt protein expression in Eca9706 cells. Notably, the PI3K agonist was able to reverse the effect of psoralidin on Eca9706 cells. The results of the present study demonstrated that psoralidin was able to inhibit proliferation and enhance apoptosis of human esophageal carcinoma cells via the NF-kappa B and PI3K/A kt signaling pathways.