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. Author manuscript; available in PMC: 2012 Apr 1.
Published in final edited form as: Cancer Res. 2011 Feb 11;71(7):2750–2760. doi: 10.1158/0008-5472.CAN-10-2954

Figure 4. LC-MRM identifies differential regulation of BIM in PTEN+ and PTEN− cell lines following PLX4720 treatment.

Figure 4

(A) Representative LC-MRM data showing the fold-changes in the expression of Bak, Bax, Bcl-2, Bcl-w, Bcl-xL, BID, BIM, Bok and Mcl-1 over internal standard in the WM164 (PTEN+) and 1205Lu (PTEN−) cell lines following treatment with PLX4720 (10μM, 0-48 hrs). Statistical analysis of BIM fold change in PTEN− versus PTEN+, *p<0.05. (B) Western blot showing BIM expression following PLX4720 treatment (10μM, 0-48 hrs) in PTEN− (WM793, 1205Lu) and WM164 cell lines (PTEN+). (C) Immunofluorescence staining, showing expression of BIM (green) and DAPI (blue) staining of PTEN− (M233, WM9, WM793, 1205Lu) and PTEN+ (WM35, WM164, WM983A) cells following PLX4720 treatment (3μM, 48 hrs). (D) Western blot showing BAD phosphorylation following treatment with PLX4720 (0-48 hrs) in PTEN− (WM793, 1205Lu) and PTEN+ WM164. Annexin V binding following treatment with 3 or 10μM PLX4720 (48 hrs) showing increased apoptosis in WM793 stably overexpressing WT BAD.