Fig 1: Bcl-xL/Bcl-2 inhibition sensitizes VS-5584-mediated activity in melanoma cells-A375 cells (A and B), primary human melanoma cells (F), B10BR murine melanocytes (G) or primary human keratinocytes (“Kera”) (G) were treated with VS-5584 (“VS”, 10 nM) or plus ABT-737 (“ABT”, 25 nM) for 72 hours, cell viability (MTT assay) and apoptosis (ELISA assay, for A375 cells) were tested.A375 cells, transfected with scramble control siRNA (sc-RNAi), Bcl-2 siRNA or Bcl-xL siRNA, were treated with VS-5584 (VS, 10 nM) for 72 hours, expression of Bcl-2, Bcl-xL and GAPDH was tested by Western blots (C, their expressions were quantified), cell survival (D) and apoptosis (E) were also tested. Data were expressed as mean ± SD, experiments were repeated three times. “C” stands for vehicle control (0.1% of DMSO). *p<0.05 vs group “C”. **p<0.05 vs “VS” only group (A, B and F). **p<0.05 vs sc-RNAi group (D and E).
Fig 2: Signaling changes by VS-5584 in melanoma cells-A375 and A-2058 cells were treated with VS-5584 (“VS”, 25 nM) or the vehicle control (1% DMSO, “C”) for 6 hours (for A and B) or 24 hours (for C), expression of listed proteins was tested by Western blots.Relative intensity of kinase phosphorylations (vs. non-phosphorylated kinases) as well as cyclin D1 and Bcl-2 expression (vs. GAPDH) of three independent experiments were shown (A-C, lower panels). Data were expressed as mean ± SD, experiments were repeated three times. *p<0.05 vs group “C”.
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