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. Author manuscript; available in PMC: 2011 Mar 16.
Published in final edited form as: Cancer Cell. 2010 Mar 16;17(3):298–310. doi: 10.1016/j.ccr.2009.12.047

Figure 4. ErbB3 is expressed and phosphorylated, and NRG1 is expressed in a subset of primary human ovarian cancers.

Figure 4

A) A subset of primary human ovarian cancer cells was analyzed for NRG1 mRNA, as detected by quantitative RT-PCR. B) ErbB3 is expressed and activated in a subset of primary human ovarian cancer cells. The p85 subunit of PI3K was co-immunoprecipitated in cells that phosphorylate ErbB3 on Y1289, consistent with active signaling through the PI3 kinase pathway. C) ErbB3 interacts with ErbB4 and Her-2 in primary DF14 ovarian cancer cells. DF14 lysates were immunoprecipitated with either control IgG or antibodies directed at either ErbB4, Her-2 or ErbB3 followed by immunoblotting with either anti-ErbB3 or anti-ErbB4. D) Conditioned medium from primary human ovarian cancer cells that intrinsically phosphorylate ErbB3 elicited ErbB3 phosphorylation and PI3K/AKT pathway activation following transfer to OVCAR5 cells. E) Top: ErbB3 directed shRNA effectively reduced ErbB3 protein expression levels in DF14 cells. Bottom: 3 different shErbB3s resulted in growth inhibition in DF14 cells. *: significantly different from sh-Control (p<0.05, student’s t-test). F) A monoclonal antibody directed against the ErbB3 ectodomain (MM-121) abolished endogenous DF14 ErbB3 phosphorylation. Error bars represent +/− SD.