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. Author manuscript; available in PMC: 2016 Oct 15.
Published in final edited form as: Mol Cell. 2015 Oct 8;60(2):307–318. doi: 10.1016/j.molcel.2015.09.002

Figure 6. EGFRvIII Sensitizes GBMs to the BET-bromodomain inhibitor JQ1.

Figure 6

(A-C) Correlation of BRD4 with SOX9, and FOXG1 in TCGA GBM gene expression data.

(D-E) Western blots indicate that BRD4 knockdown decreases c-MYC in U87EGFRvIII cells. JQ1 treatment (1 μM) for 48 hrs decreases c-MYC while increasing the level of BRD4, suggesting that BRD4 histone-binding activity is essential for the expression of c-MYC.

(F-G) Western blots show that BRD4 and c-MYC are depleted by SOX9 or FOXG1 knockdown in U87EGFRvIII cells. (H) Annexin V/PI FACS analysis of apoptotic cells in a series of stable cell lines following 5-day treatment with 1 μM JQ1. U87EGFRvIII cells experienced significantly higher apoptosis levels compared to all the other cell lines. **: p <0.01, ***: p <0.001, ANOVA test with Dunnett's multiple comparison test. Error bars represent S.D.

(I) Heightened sensitivity to JQ1 relies on EGFRvIII's kinase activity. **: p<0.01, ***: p<0.001, N.S.: not significant. t-test. Error bars represent SD.

(J-K) Inducible EGFRvIII-expressing GBM cell lines are sensitive to JQ1-induced apoptosis. **: p<0.01, N.S.: not significant. t-test. Error bars represent SD.

See also Figure S6.