Title : MYC-Regulated Mevalonate Metabolism Maintains Brain Tumor-Initiating Cells.

Pub. Date : 2017 Sep 15

PMID : 28729418






6 Functional Relationships(s)
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1 MYC-Regulated Mevalonate Metabolism Maintains Brain Tumor-Initiating Cells. Mevalonic Acid MYC proto-oncogene, bHLH transcription factor Homo sapiens
2 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. Mevalonic Acid MYC proto-oncogene, bHLH transcription factor Homo sapiens
3 BTICs preferentially express mevalonate pathway enzymes, which we find regulated by novel MYC-binding sites, validating an additional transcriptional activation role of MYC in cancer metabolism. Mevalonic Acid MYC proto-oncogene, bHLH transcription factor Homo sapiens
4 BTICs preferentially express mevalonate pathway enzymes, which we find regulated by novel MYC-binding sites, validating an additional transcriptional activation role of MYC in cancer metabolism. Mevalonic Acid MYC proto-oncogene, bHLH transcription factor Homo sapiens
5 In turn, mevalonate created a positive feed-forward loop to activate MYC signaling via induction of miR-33b. Mevalonic Acid MYC proto-oncogene, bHLH transcription factor Homo sapiens
6 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. Mevalonic Acid MYC proto-oncogene, bHLH transcription factor Homo sapiens