Decreasing Galectin-1 Expression in Human Hs683 Glioblastoma Cells Impairs their Response to Endoplasmic Reticulum Stress

摘要: Glioblastomas (GBMs) are resistant to apoptosis, but not autophagy, a fact that can, at least partly, explain the therapeutic benefits of pro-autophagic drug temozolomide in treatment GBM patients. Galectin-1 is potent modulator cell migration and close partner Ras, whose importance as signaling molecule case GBMs has already been highlighted. The data present study show depletion by anti-galectin-1 siRNA galectin-1 expression human Hs683 cells does induce apoptotic or autophagic features. In contrast, this decreases levels several genes involved response endoplasmic reticulum (ER) stress (ERS), including DUSP5, HERP, DNAJB9/MDG1/Erdj4 ORP150/HYOU1, latter which modulates angiogenesis via processing VEGF. tumor leads sustained VEGF expression, with severe vivo impairments orthotopic xenografts. delivery non-viral infusion into ventricular system brains adult mice orthotopically grafted increases anti-tumor effects temozolomide. This novel facet involvement glioblastoma biology may be amenable manipulation.