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XBP1 silencing decreases glioma cell viability and glycolysis possibly by inhibiting HK2 expression

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Abstract

Glioma cells rely on glycolysis to obtain energy and sustain their survival under microenvironmental stress in vivo. The mechanisms of regulation of glycolysis in glioma cells are unclear. Signaling pathway mediated by the transcription factor X box-binding protein 1 (XBP1) is one of the most important pathways of unfolded protein response which is comprehensively activated in cancer cells upon the microenvironmental stress. Here we showed that XBP1 was significantly activated in glioma tissues in vivo. XBP1 silencing resulted in decreasing of glioma cell viability and ATP/lactate production under hypoxia, which is possibly mediated by inhibition of Hexokinase II (HK2)’s expression. More importantly, XBP1 silenced glioma cells showed the decrease of tumor formation capacity. Our results revealed that XBP1s activation was involved in glioma glycolysis regulation and might be a potential molecular target for glioma treatment.

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Acknowledgments

The funding of this study was supported by the National Natural Science Foundation of China (No. 81172388 and 81372701 to Yaohua Liu, No. 81272788 to Shiguang Zhao).

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Correspondence to Shiguang Zhao.

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The authors have declared that no conflict of interest exist.

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Yaohua Liu, Xu Hou and Min Liu have contributed equally to this work.

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Liu, Y., Hou, X., Liu, M. et al. XBP1 silencing decreases glioma cell viability and glycolysis possibly by inhibiting HK2 expression. J Neurooncol 126, 455–462 (2016). https://doi.org/10.1007/s11060-015-2003-y

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  • DOI: https://doi.org/10.1007/s11060-015-2003-y

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