Zhao Xin, Feng Xia, Wang Cun, Peng Deguang, Zhu Kai, Song Jia-Le
Chongqing Collaborative Innovation Center for Functional Food, Chongqing University of Education, Chongqing 400067, P.R. China.
Chongqing Enterprise Engineering Research Center of Ba-lotus Breeding and Deep Processing, Chongqing 400041, P.R. China.
Oncol Lett. 2017 Mar;13(3):1470-1478. doi: 10.3892/ol.2016.5547. Epub 2016 Dec 28.
The aim of the present study was to investigate the anticancer activities of (Ba lotus) stamen ethanol crude extract (BLSEE) in human colon carcinoma HCT-116 cells. MTT assay, flow cytometry analysis and reverse transcription-polymerase chain reaction assay were employed to investigate the anticancer mechanisms of BLSEE (100, 200 and 400 µg/ml) in HCT-116 cells. BLSEE reduced HCT-116 cell proliferation in a dose-dependent manner. BLSEE treatment also significantly increased the sub-G1 population in HCT-116 cells (P=0.0020 at 400 µg/ml), as shown by flow cytometry assay. Following treatment with BLSEE, the mRNA levels of the apoptosis-associated factors Fas, Fas ligand, tumor necrosis factor-related apoptosis-inducing ligand, death receptor 4 (DR4), death receptor 5 (DR5), caspases 3, 8 and 9, and B-cell lymphoma-2 (Bcl-2) associated X protein were increased, and the expression of anti-apoptotic Bcl-2 and Bcl-extra large was decreased in HCT-116 cells. The mRNA levels of matrix metalloproteinase (MMP)-2, MMP-9, TIMP metallopeptidase inhibitor 1 and TIMP metallopeptidase inhibitor 2 were also regulated by BLSEE treatment. In addition, BLSEE was able to modulate the expression of inflammation-associated nuclear factor-κB, inhibitory κBα, inducible nitric oxide synthase and cyclooxygenase 2 in HCT-116 cells. The present study clearly indicated the cytotoxicity of BLSEE in HCT-116 cells through induced cellular apoptosis. These results also suggested the BLSEE may be a powerful agent against colon cancer cells.
本研究的目的是调查(巴荷花)雄蕊乙醇粗提物(BLSEE)对人结肠癌HCT - 116细胞的抗癌活性。采用MTT法、流式细胞术分析和逆转录 - 聚合酶链反应法研究BLSEE(100、200和400μg/ml)在HCT - 116细胞中的抗癌机制。BLSEE以剂量依赖性方式降低HCT - 116细胞增殖。流式细胞术检测显示,BLSEE处理还显著增加了HCT - 116细胞中的亚G1期细胞群(400μg/ml时P = 0.0020)。用BLSEE处理后,HCT - 116细胞中凋亡相关因子Fas、Fas配体、肿瘤坏死因子相关凋亡诱导配体、死亡受体4(DR4)、死亡受体5(DR5)、半胱天冬酶3、8和9以及B细胞淋巴瘤 - 2(Bcl - 2)相关X蛋白的mRNA水平升高,抗凋亡蛋白Bcl - 2和Bcl - 2超大蛋白的表达降低。基质金属蛋白酶(MMP)-2、MMP - 9、TIMP金属肽酶抑制剂1和TIMP金属肽酶抑制剂2的mRNA水平也受到BLSEE处理的调节。此外,BLSEE能够调节HCT - 116细胞中炎症相关核因子 - κB、抑制性κBα、诱导型一氧化氮合酶和环氧化酶2的表达。本研究清楚地表明BLSEE通过诱导细胞凋亡对HCT - 116细胞具有细胞毒性。这些结果还表明BLSEE可能是一种对抗结肠癌细胞的有力药物。