Journal
SCIENTIFIC REPORTS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep25956
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Funding
- NIH [U01 CA141502, U54 CA143798, U54CA163167, RO1 CA94842]
- Commonwealth Foundation for Cancer Research
- Experimental Therapeutics Center of MSKCC
- William Randolph Hearst Fund in Experimental Therapeutics
- Lillian S Wells Foundation
- NIH/NCI Cancer Center [5 P30 CA008748-44]
- Tegger Foundation
- Swedish Research Council
- Swedish Childhood Cancer Foundation
- Swedish Cancer Society
- Italian Ministry of Health [GR 2010 2312023]
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Glioma cells with stem cell traits are thought to be responsible for tumor maintenance and therapeutic failure. Such cells can be enriched based on their inherent drug efflux capability mediated by the ABC transporter ABCG2 using the side population assay, and their characteristics include increased self-renewal, high stem cell marker expression and high tumorigenic capacity in vivo. Here, we show that ABCG2 can actively drive expression of stem cell markers and self-renewal in glioma cells. Stem cell markers and self-renewal was enriched in cells with high ABCG2 activity, and could be specifically inhibited by pharmacological and genetic ABCG2 inhibition. Importantly, despite regulating these key characteristics of stem-like tumor cells, ABCG2 activity did not affect radiation resistance or tumorigenicity in vivo. ABCG2 effects were Notch-independent and mediated by diverse mechanisms including the transcription factor Mef. Our data demonstrate that characteristics of tumor stem cells are separable, and highlight ABCG2 as a potential driver of glioma stemness.
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