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. Author manuscript; available in PMC: 2015 Sep 15.
Published in final edited form as: Clin Cancer Res. 2014 Jul 28;20(18):4849–4860. doi: 10.1158/1078-0432.CCR-14-0034

Fig. 4. Ectopic expression of constitutively active AKT or inhibition of GSK3 diminishes BEZ235/panobinostat lethality.

Fig. 4

A) Western blot on constitutively active Myc-tagged AKT-expressing SU-DHL16 cells following 24 hr exposure to 25 nM BEZ235 ± 7.5 nM panobinostat. Alternatively, the extent of cell death (B) or cell growth and viability (C) were assessed at 24 hr as in Fig. 1A-B. Error Bars: S.D of 3 independent experiments; * P < 0.02. D) SU-DHL4, SU-DHL16, HBL-1, and OCI-LY18 cells were treated with BEZ235 (200 nM for SU-DHL4, HBL-1, and OCI-LY18; 25 nM for SU-DHL16) ± panobinostat (7.5 nM for SU-DHL16; 10 nM for HBL-1, and OCI-LY18; 15 nM for SU-DHL4) for 8 hr, then cells were lysed and Western blot performed using the indicated antibodies. E) SU-DHL4 and HBL-1 cells were exposed to combined treatment with BEZ235 and panobinostat as in (D) in the presence or the absence of BIO, MeBIO, or CHIR-98014 (2 μM each). Twenty-four hr after treatment, cell growth and viability were assessed using CellTiter-Glo Luminescent assay. * = significantly greater than values obtained in the absence of BIO or CHIR-98014 (P < 0.05).