Fig. 2
From: Oncogenic fusion proteins adopt the insulin-like growth factor signaling pathway
Regulation of IGF1R gene expression by aberrant transcription factor TMPRSS2-ERG in prostate cancer cells. a M12 cells (lacking the fusion protein) were infected with an ERG-encoding viral vector. Cells were lysed, electrophoresed through SDS-PAGE, followed by transfer and incubation with an IGF1R β subunit antibody. ERG expression leads to enhancement of both the mature (100-kDa) and precursor (250-kDa) forms of IGF1R. VCaP cells (expressing TMPRSS2-ERG) were transfected with a siRNA directed against the fusion protein (siERG), or control non-targeting (NT) siRNA. Cells were harvested after 96 h and levels of T-ERG and IGF1R were measured by Western blots. Data indicate that ERG silencing led to a reduction in mature IGF1R levels. b M12 cells were cotransfected with an IGF1R promoter-luciferase reporter, along with an ERG expression vector (or empty vector), and VCaP cells were cotransfected with the IGF1R luciferase reporter, along with siERG or NT siRNA. Luciferase activity was measured after 48 h and normalized to β-galactosidase values. Results indicate that ERG stimulated IGF1R gene transcription [83]