Jin Zhiliang, Yan Wei, Jin Hui, Ge Changzheng, Xu Yanhua
Department of Oncology, Central Hospital of Jingzhou, Jingzhou, Hubei 434020, P.R. China.
Department of Gastroenterology, Central Hospital of Jingzhou, Jingzhou, Hubei 434020, P.R. China.
Oncol Lett. 2016 Jan;11(1):267-272. doi: 10.3892/ol.2015.3861. Epub 2015 Nov 4.
Worldwide, colon cancer is the third most common cancer in terms of incidence, following lung and breast cancer. Resistance to psoralidin frequently occurs following its use as an anticancer treatment. However, the mechanisms underlying the effects of psoralidin on colon cancer, remain to be elucidated. Hence, the present study investigated the anticancer effects and potential mechanism of action of psoralidin on SW480 human colon cancer cells. In the present study, an MTT assay was performed to measure the viability of SW480 cells. Additionally, an Annexin V-fluorescein isothiocyanate/propidium iodide apoptosis detection kit, DAPI staining assay and caspase-3 colorimetric assay kits were used to analyze the cellular apoptosis of SW480 cells. The nuclear factor-κB (NF-κB) p65 activity and B-cell lymphoma-2 (Bcl-2)/Bcl-2-associated X protein (Bax) protein expression of SW480 cells was detected using NF-κB colorimetric assay kits and western blot analysis, respectively. Bcl-2 inhibitor ABT-737 was added to SW480 cells and the subsequent effects and mechanism of action of psoralidin on SW480 colon cancer cells was studied. In the present study, psoralidin reduced SW480 cell viability and enhanced the cellular apoptosis of SW480 cells in a dose-dependent manner. Caspase-3 activity of SW480 cells was increased following treatment with psoralidin. Additionally, psoralidin was able to reduce the NF-κB p65 activity of SW480 cells. Furthermore, psoralidin was able to reduce Bcl-2 protein expression and increase Bax protein expression in SW480 cells. Notably, Bcl-2 inhibitor was observed to enhance the effects of psoralidin on SW480 cells. The results of the present study suggest that psoralidin may be a candidate drug for the treatment of colon cancer by inhibition of the NF-κB and Bcl-2/Bax signaling pathways.
在全球范围内，就发病率而言，结肠癌是第三大常见癌症，仅次于肺癌和乳腺癌。补骨脂素用作抗癌治疗后，经常会出现耐药性。然而，补骨脂素对结肠癌作用的潜在机制仍有待阐明。因此，本研究调查了补骨脂素对SW480人结肠癌细胞的抗癌作用及其潜在作用机制。在本研究中，进行了MTT试验以测量SW480细胞的活力。此外，使用膜联蛋白V-异硫氰酸荧光素/碘化丙啶凋亡检测试剂盒、DAPI染色试验和半胱天冬酶-3比色测定试剂盒分析SW480细胞的细胞凋亡。分别使用NF-κB比色测定试剂盒和蛋白质印迹分析检测SW480细胞的核因子-κB（NF-κB）p65活性和B细胞淋巴瘤-2（Bcl-2）/Bcl-2相关X蛋白（Bax）蛋白表达。将Bcl-2抑制剂ABT-737添加到SW480细胞中，并研究补骨脂素对SW480结肠癌细胞的后续作用及其作用机制。在本研究中，补骨脂素以剂量依赖性方式降低SW480细胞活力并增强SW480细胞的细胞凋亡。用补骨脂素处理后，SW480细胞的半胱天冬酶-3活性增加。此外，补骨脂素能够降低SW480细胞的NF-κB p65活性。此外，补骨脂素能够降低SW480细胞中Bcl-2蛋白表达并增加Bax蛋白表达。值得注意的是，观察到Bcl-2抑制剂可增强补骨脂素对SW480细胞的作用。本研究结果表明，补骨脂素可能是一种通过抑制NF-κB和Bcl-2/Bax信号通路来治疗结肠癌的候选药物。
