Physcion 8-O-β-glucopyranoside (PG), the main active ingredient of Rumex japonicus, induces apoptosis and causes cell cycle arrest in human lung cancer cells. However, its anti-tumor effects are not fully understood. In this study, we explored the mechanisms underlying PG induced apoptosis in the osteosarcoma cell line MG-63. Our results showed that PG exerted anti-proliferative effects and induced apoptosis in MG-63 cells via the intrinsic mitochondrial pathway, accompanied by loss of mitochondrial membrane potential (MMP) and cytochrome C release from the mitochondria. In addition, physcion treatment significantly inhibited extracellular matrix metalloproteinase inducer (EMMPRIN) expression in MG-63 cells, in a dose-dependent manner; meanwhile, EMMPRIN protein overexpression markedly reduced PG-induced apoptosis. Moreover, our findings suggested that the modulatory effects of PG on EMMPRIN were due, at least in part, to regulation of an ROS-miR-27a/ZBTB10-Sp1 transcription factor pathway.

译文

:Physicion8-O-β-吡喃葡萄糖苷(PG)是Rumex japonicus的主要活性成分,可诱导人肺癌细胞凋亡并引起细胞周期停滞。但是,其抗肿瘤作用尚未完全了解。在这项研究中,我们探讨了PG诱导骨肉瘤细胞MG-63凋亡的潜在机制。我们的研究结果表明,PG通过内在的线粒体途径发挥抗增殖作用并诱导MG-63细胞凋亡,并伴随着线粒体膜电位(MMP)的丧失和线粒体中细胞色素C的释放。另外,physcion处理以剂量依赖的方式显着抑制MG-63细胞中的细胞外基质金属蛋白酶诱导剂(EMMPRIN)的表达。同时,EMMPRIN蛋白的过表达显着降低了PG诱导的细胞凋亡。此外,我们的发现表明,PG对EMMPRIN的调节作用至少部分归因于ROS-miR-27a / ZBTB10-Sp1转录因子途径的调节。

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