| Popis: |
Gypenosides (Gyp), a Chinese medicine and an effective ingredient extracted from Gynostemma pentaphyllum, plays vital roles in the progression of various cancers. However, its biological functions and mechanisms in glioma remain unclear. We evaluated the anti-cancer mechanism of Gyp in glioma to determine its potential therapeutic value. In human glioma cells, we evaluated cell viability using MTS assays and cell mobility using Transwell invasion and scratch migration assays. Additionally, we assessed apoptosis using flow cytometry and Hoechst 33342 staining, and autophagy flow was detected by Fluorescence microscope. The levels of migration, apoptosis and autophagy-related protein were examinated by Western blot. Gyp inhibited the proliferation, migration and invasion of glioma cells by down-regulating the level of matrix metalloproteinase (MMP)-2 and MMP-9. Moreover, Gyp promoted apoptosis of glioma cells by inducing Bax and cleaved-caspase-9 activation and down-regulating Bcl-2. Notably, autophagy was activated by treating with Gyp in U251 and U87 cells through down-regulation of p62 protein and up-regulation of Beclin1 and LC3 II proteins. Interestingly, treatment with autophagy flux inhibitor Baf-A1 or 3-MA blocked the inhibitory effects of Gyp in glioma cells. Combined application of Gyp with Baf-A1 or 3-MA slightly increased cell death, suggesting that induction of autophagy impaired enzyme accumulation and contributed to the growth inhibition of glioma cells. In summary, Gyp suppressed the proliferation, migration and invasion and induced apoptosis of glioma cells by promoting autophagy, suggested the potential value of Gyp in the combined treatment of glioma. |
