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phospho igf 1rb 3024 antibodies  (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc phospho igf 1rb 3024 antibodies
Fig. 4. Blocking IGF-1R prevents drug washout mediated cancer cell growth. (A) Washout of PI3K or mTOR inhibitors increases <t>IGF-1Rb</t> phosphorylation. HT-29 cells were treated for six hours with DMSO, BYL719 (10 mM) (BYL), BKM-120 (500 nM) (BKM), PP242 (5 mM) or Ku0063794 (5 mM) (Ku). Following washout, cells were incubated for six hours, and cell lysates were collected and analyzed for IGF-1Rb phosphorylation and actin. (B) IGF-1R inhibition with NVP-AEW541 blocks AKT phosphorylation mediated by washout of PP242 or BKM-120. HT-29 cells were treated with DMSO, PP242 (5 mM) or BKM-120 (500 mM) for 6 h. Following drug washout, cells were treated as indicated with sapitinib (2 mM), NVP- AEW541 (1 mM) (NVP-AEW) or erlotinib (1 mM) for six hours, and AKT phosphorylation was assessed by Western blot in cell lysates. (C) NVP-AEW541 inhibits cancer cell pro- liferation induced by washout of PP242 or BKM-120. HT-29 cells were treated with DMSO, PP242 (5 mM) or BKM-120 (500 nM) for six hours. Following drug washout, cells were incubated with DMSO or NVP-AEW541 (1 mM) for an additional 48 h. Cell proliferation was assessed with an MTS proliferation assay. Columns: Mean cell proliferation of three independent experiments expressed as percentage of DMSO treated cancer cells. Bars: SD. White columns: DMSO treated cells, grey columns: cells treated with PP242, and black columns: cells treated with BKM-120. *p < 0.05 compared to control cells.
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Fig. 4. Blocking IGF-1R prevents drug washout mediated cancer cell growth. (A) Washout of PI3K or mTOR inhibitors increases IGF-1Rb phosphorylation. HT-29 cells were treated for six hours with DMSO, BYL719 (10 mM) (BYL), BKM-120 (500 nM) (BKM), PP242 (5 mM) or Ku0063794 (5 mM) (Ku). Following washout, cells were incubated for six hours, and cell lysates were collected and analyzed for IGF-1Rb phosphorylation and actin. (B) IGF-1R inhibition with NVP-AEW541 blocks AKT phosphorylation mediated by washout of PP242 or BKM-120. HT-29 cells were treated with DMSO, PP242 (5 mM) or BKM-120 (500 mM) for 6 h. Following drug washout, cells were treated as indicated with sapitinib (2 mM), NVP- AEW541 (1 mM) (NVP-AEW) or erlotinib (1 mM) for six hours, and AKT phosphorylation was assessed by Western blot in cell lysates. (C) NVP-AEW541 inhibits cancer cell pro- liferation induced by washout of PP242 or BKM-120. HT-29 cells were treated with DMSO, PP242 (5 mM) or BKM-120 (500 nM) for six hours. Following drug washout, cells were incubated with DMSO or NVP-AEW541 (1 mM) for an additional 48 h. Cell proliferation was assessed with an MTS proliferation assay. Columns: Mean cell proliferation of three independent experiments expressed as percentage of DMSO treated cancer cells. Bars: SD. White columns: DMSO treated cells, grey columns: cells treated with PP242, and black columns: cells treated with BKM-120. *p < 0.05 compared to control cells.

Journal: Biochemical and biophysical research communications

Article Title: Rebound pathway overactivation by cancer cells following discontinuation of PI3K or mTOR inhibition promotes cancer cell growth.

doi: 10.1016/j.bbrc.2019.04.044

Figure Lengend Snippet: Fig. 4. Blocking IGF-1R prevents drug washout mediated cancer cell growth. (A) Washout of PI3K or mTOR inhibitors increases IGF-1Rb phosphorylation. HT-29 cells were treated for six hours with DMSO, BYL719 (10 mM) (BYL), BKM-120 (500 nM) (BKM), PP242 (5 mM) or Ku0063794 (5 mM) (Ku). Following washout, cells were incubated for six hours, and cell lysates were collected and analyzed for IGF-1Rb phosphorylation and actin. (B) IGF-1R inhibition with NVP-AEW541 blocks AKT phosphorylation mediated by washout of PP242 or BKM-120. HT-29 cells were treated with DMSO, PP242 (5 mM) or BKM-120 (500 mM) for 6 h. Following drug washout, cells were treated as indicated with sapitinib (2 mM), NVP- AEW541 (1 mM) (NVP-AEW) or erlotinib (1 mM) for six hours, and AKT phosphorylation was assessed by Western blot in cell lysates. (C) NVP-AEW541 inhibits cancer cell pro- liferation induced by washout of PP242 or BKM-120. HT-29 cells were treated with DMSO, PP242 (5 mM) or BKM-120 (500 nM) for six hours. Following drug washout, cells were incubated with DMSO or NVP-AEW541 (1 mM) for an additional 48 h. Cell proliferation was assessed with an MTS proliferation assay. Columns: Mean cell proliferation of three independent experiments expressed as percentage of DMSO treated cancer cells. Bars: SD. White columns: DMSO treated cells, grey columns: cells treated with PP242, and black columns: cells treated with BKM-120. *p < 0.05 compared to control cells.

Article Snippet: Anti-phospho-AKT (#4060), anti-AKT (#2920), and anti phospho-IGF-1Rb (#3024) antibodies were from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Blocking Assay, Phospho-proteomics, Incubation, Inhibition, Western Blot, Proliferation Assay, Control