Journal
CANCER CELL
Volume 29, Issue 1, Pages 49-60Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2015.12.005
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Funding
- NIH [CA164791, AI091878]
- National Natural Science Foundation of China [81201978, 81200362]
- Natural Science Foundation of Jiangsu Province [BK2012483]
- Program for Advanced Talents within Six Industries of Jiangsu Province [2012-WSN-019]
- Duke University Brain Cancer SPORE
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The hypoxic tumor microenvironment serves as a niche for maintaining the glioma-initiating cells (GICs) that are critical for glioblastoma (GBM) occurrence and recurrence. Here, we report that hypoxia-induced miR-215 is vital for reprograming GICs to fit the hypoxic microenvironment via suppressing the expression of an epigenetic regulator KDM1B and modulating activities of multiple pathways. Interestingly, biogenesis of miR-215 and several miRNAs is accelerated post-transcriptionally by hypoxia-inducible factors (HIFs) through HIF-Drosha interaction. Moreover, miR-215 expression correlates inversely with KDM1B while correlating positively with HIF1 alpha and GBM progression in patients. These findings reveal a direct role of HIF in regulating miRNA biogenesis and consequently activating the miR-215-KDM1B-mediated signaling required for GIC adaptation to hypoxia.
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