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MYC-Regulated Mevalonate Metabolism Maintains Brain Tumor-Initiating Cells
Journal article   Open access   Peer reviewed

MYC-Regulated Mevalonate Metabolism Maintains Brain Tumor-Initiating Cells

Xiuxing Wang, Zhi Huang, Qiulian Wu, Briana C. Prager, Stephen C. Mack, Kailin Yang, Leo J. Y. Kim, Ryan C. Gimple, Yu Shi, Sisi Lai, …
Cancer research (Chicago, Ill.), Vol.77(18), pp.4947-4960
09/15/2017
DOI: 10.1158/0008-5472.CAN-17-0114
PMCID: PMC5600855
PMID: 28729418
url
https://doi.org/10.1158/0008-5472.CAN-17-0114View
Published (Version of record) Open Access

Abstract

Metabolic dysregulation drives tumor initiation in a subset of glioblastomas harboring isocitrate dehydrogenase (IDH) mutations, but metabolic alterations in glioblastomas with wild-type IDHare poorly understood. MYCpromotes metabolic reprogramming in cancer, but targeting MYC has proven notoriously challenging. Here, we link metabolic dysregulation in patient-derived brain tumor-initiating cells (BTIC) to a nexus between MYC and mevalonate signaling, which can be inhibited by statin or 6-fluoromevalonate treatment. BTICs preferentially express meva-lonate pathway enzymes, which we find regulated by novel MYC-binding sites, validating an additional transcriptional activation role of MYC in cancer metabolism. Targeting mevalonate activity attenuated RAS-ERK-dependent BTIC growth and self-renewal. In turn, mevalonate created a positive feed-forward loop to activate MYC signaling via induction of miR-33b. Collectively, our results argue that MYC mediates its oncogenic effects in part by altering mevalonate metabolism in glioma cells, suggesting a therapeutic strategy in this setting. (C)2017 AACR.
Life Sciences & Biomedicine Oncology Science & Technology

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