The First Clinical Medicine School, Nanjing University of Chinese Medicine (NUCM), China.
Acta Biochim Biophys Sin (Shanghai). 2011 Sep;43(9):698-702. doi: 10.1093/abbs/gmr063. Epub 2011 Jul 23.
Neogambogic acid (NGA), an active ingredient in garcinia, can inhibit the growth of some solid tumors and result in an anticancer effect. We hypothesize that NGA may be responsible for the inhibition of proliferation of human breast cancer cell line MCF-7 cells. To investigate its anticancer mechanism in vitro, MCF-7 cells were treated with various concentrations of NGA. Results of MTT (methyl thiazolyl tetrazolum) assay showed that treatment with NGA significantly reduced the proliferation of MCF-7 cells in a dose-dependent manner. NGA could increase the expression of the apoptosis-related proteins FasL, caspase-3, caspase-8, caspase-9, and Bax and decrease the expression of anti-apoptotic protein Bcl-2 accompanied by the mitochondrial transmembrane damage. The antiproliferative effect of NGA on MCF-7 cells is due to the G(0)/G(1) arrest, increased apoptosis and activation of Fas/FasL and cytochrome C pathway. These results provide an important insight into the cellular and molecular mechanisms through which NGA impairs the proliferation of breast cancer cells.
新藤黄酸（NGA）是藤黄中的一种活性成分，能够抑制某些实体肿瘤的生长，从而产生抗癌作用。我们假设 NGA 可能是抑制人乳腺癌 MCF-7 细胞增殖的原因。为了研究其体外抗癌机制，用不同浓度的 NGA 处理 MCF-7 细胞。MTT（噻唑蓝）检测结果表明，NGA 处理以剂量依赖的方式显著降低 MCF-7 细胞的增殖。NGA 能够增加凋亡相关蛋白 FasL、caspase-3、caspase-8、caspase-9 和 Bax 的表达，降低抗凋亡蛋白 Bcl-2 的表达，并伴有线粒体跨膜损伤。NGA 对 MCF-7 细胞的增殖抑制作用是由于 G(0)/G(1) 期阻滞、凋亡增加以及 Fas/FasL 和细胞色素 C 通路的激活。这些结果为 NGA 损害乳腺癌细胞增殖的细胞和分子机制提供了重要的见解。
