Cai Qiaoyan, Lin Jing, Zhang Ling, Lin Shan, Peng Jun
Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
Fujian Key Laboratory of Integrative Medicine on Geriatrics, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
Oncol Lett. 2018 Jun;15(6):8871-8877. doi: 10.3892/ol.2018.8366. Epub 2018 Mar 28.
The chloroform fraction of the folk Chinese medicine, (CSC) and its anti-inflammatory activity is well recognized. However, the molecular mechanisms underlying the beneficial anticancer effects of CSC remain largely unknown. The aim of the present study was to examine the effects of CSC on the regulation of cell proliferation and apoptosis in SGC-7901 gastric cancer cells, as well as to investigate the underlying molecular mechanisms involved. The results from the present study demonstrated that CSC treatment inhibited SGC-7901 cell viability and survival in a dose- and/or time-dependent manner. CSC treatment further induced the apoptosis of SGC-7901 cells, characterized by distinct chromatin condensation and fragmented nuclear morphology. In addition, CSC treatment suppressed protein kinase-B (Akt) phosphorylation and phosphatidylinositide 3-kinase (PI3K) expression in SGC-7901 cells, which in turn promoted cancer cell apoptosis and inhibited cell proliferation. Furthermore, CSC treatment altered the expression pattern of several key target genes of the PI3K/Akt signaling pathway through the downregulation of Cyclin D1, cyclin-dependent kinase-4 and B-cell lymphoma-2 and the upregulation of Bcl-2-associated X protein. Therefore, the results from the present study demonstrated that CSC suppressed cell survival and induced apoptosis in human gastric cancer cells, via targeting the PI3K/Akt pathway.
中国民间药物(CSC)的氯仿提取物及其抗炎活性已得到充分认可。然而,CSC有益抗癌作用的分子机制仍 largely未知。本研究的目的是研究CSC对SGC - 7901胃癌细胞增殖和凋亡调控的影响,并探讨其潜在的分子机制。本研究结果表明,CSC处理以剂量和/或时间依赖性方式抑制SGC - 7901细胞活力和存活。CSC处理进一步诱导SGC - 7901细胞凋亡,其特征为明显的染色质浓缩和核形态碎片化。此外,CSC处理抑制SGC - 7901细胞中蛋白激酶B(Akt)磷酸化和磷脂酰肌醇3 -激酶(PI3K)表达,进而促进癌细胞凋亡并抑制细胞增殖。此外,CSC处理通过下调细胞周期蛋白D1、细胞周期蛋白依赖性激酶4和B细胞淋巴瘤-2以及上调Bcl-2相关X蛋白,改变了PI3K/Akt信号通路几个关键靶基因的表达模式。因此,本研究结果表明,CSC通过靶向PI3K/Akt途径抑制人胃癌细胞的存活并诱导凋亡。