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. Author manuscript; available in PMC: 2010 May 15.
Published in final edited form as: Cancer Res. 2009 May 12;69(10):4192–4201. doi: 10.1158/0008-5472.CAN-09-0042

Fig. 5. PTEN loss prolongs IGF-IR and HER3 signaling, and increases E2-induced non-genomic signaling via IGF-IR.

Fig. 5

A) p85 was immunoprecipitated from lysates of MCF-7 cells that had been pretreated overnight with serum-free medium +/− AEW541 (1 µM), then stimulated +/− 100 ng/mL IGF-I +/− AEW541 × 5, 60, or 180 min. Arrowhead indicates P-IGF-IRβ. B) Lysates from MCF-7 cells pretreated as in (A) +/− AEW541 (1 µM) or lapatinib (1 µM), then stimulated +/− IGF-I (100 ng/mL) +/− inhibitors × 15 min. C) p85 was immunoprecipitated from lysates of T47D cells treated with 0.5% DCC-FBS +/− lapatinib [1 µM × 15, 30, 60, 120, or 180 min., or overnight (o/n)]. Short and long exposures (exp) for P-HER3 are shown. D) p85 was immunoprecipitated from lysates of MCF-7 cells pretreated overnight with 10% DCC-FBS +/− 1 µM 4-OH-T, 1 µM fulvestrant, 1 µM AEW541, or 1 µM lapatinib, and then stimulated +/− 1 nM E2 +/− inhibitors × 20 min. Arrowhead indicates tyr-phosphorylated IRS-1 (≈150 kDa). All immunoprecipitates and cell lysates were analyzed by immunoblotting with the indicated antibodies.