Objective:To determine the effect of hypoxic stress on glioma cell XBP1 expression, the relationship between XBP1 expres-sion and sugar metabolism, the influence of XBP1 repression on the survival rate of glioma cells under normoxia and hypoxia, and the influence of XBP1 on glioma cell glycolysis. Methods:We tested XBP1 activation in human glioma cell lines cultured under normoxia and hypoxia. XBP1 expression was repressed with siRNA technology. Cells were treated with oxidative phosphorylation inhibitor. We then detected the variation in cell apoptosis, sugar metabolism mode, and cell apoptosis and glycolysis products under normoxia and hypoxia. Results:XBP1 activation increased under hypoxia. Silencing XBP1 expression reduced glioma cell survival level, ATP and lactic acid production, and glucose consumption under hypoxia. After inhibiting cell oxidative phosphorylation, XBP1 repression significantly reduced the survival level of glioma cells. Conclusion:Hypoxia can activate XBP1 in glioma cells. Under hypoxia, XBP1 silencing de-presses cell activity and glycolysis. Glycolysis of glioma cells under hypoxia depends on XBP1 activation.

During growth,invasion and metastasis,tumor cells undergo endoplasmic reticulum stress(ERS)under hypoxia,hy-poglycemia and other environmental stresses.In response to ERS,tumor cells induce unfolded protein response(UPR).PERK signa-ling pathway as a key pathway to activate UPR can promote survival,proliferation,invasion and protection of tumor cells by increasing tumor tolerance to adverse microenvironment,inducting angiogenesis,inducing autophagosome formation and activating apoptotic signal molecules.Tumor cells are induced apoptotic and autophagic death when UPR reaches a certain extent.