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. Author manuscript; available in PMC: 2016 Mar 24.
Published in final edited form as: Cell Rep. 2015 Mar 12;10(11):1899–1912. doi: 10.1016/j.celrep.2015.02.041

Figure 7. Abcg1 expression maintains o-GSC growth.

Figure 7

(A) Glioma specimens from six individuals with NF1 exhibit ABCG1 expression relative to age-matched control brains. Scale bar, 50 μm. (B) shRNA knockdown of o-GSC Abcg1 expression. shAbcg1 knockdown reduced (C) o-GSC growth and (D) decreased self-renewal. Scale bar, 200 μm. Following Abcg1 knockdown, there was (E) no change in proliferation (% Ki67+ cells); however, and (F) increased apoptosis (% TUNEL+ cells) were observed. (G, H) Abcg1 knockdown induced caspase-3, caspase-6, caspase-12, and PARP, but not caspase-9, cleavage. (I) Increased BiP and CHOP expression was observed following Abcg1 knockdown. Tunicamycin (TM) (2μg/ml) was included as a control to induce ER stress. (J) Expression of BiP, CHOP, cleaved-caspase-3 and cleaved-PARP was decreased following Abcg1 knockdown in o-GSCs treated with PBA (2mM), an ER stress inhibitor. (K) Proposed mechanism underlying Abcg1 maintenance of o-GSC survival through suppression of ER stress. Error bars denote mean ± SD. NS, not significant. (*) p<0.01.