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. 2008 Feb;10(2):177–188. doi: 10.1593/neo.07822

Figure 3.

Figure 3

Knockdown of ERG in VCaP cells attenuates a transcriptional program over-expressed in TMPRSS2-ETS-positive prostate cancers. (a) SiRNA knockdown of ERG in the TMPRSS2-ERG-positive prostate cancer cell line VCaP. VCaP cells were treated with transfection reagent alone (untreated), or transfected with nontargeting or ERG siRNA (VCaP-siERG) as indicated. ERG knockdown was confirmed by immunoblot analysis. (b) VCaP cells as indicated were assayed for invasion through a modified basement membrane. (c) VCaP-siERG and VCaP cells treated with nontargeting siRNA were profiled and a molecular concept map of the under-expressed in VCaP-siERG signature (ringed yellow node) was generated. Each edge represents a significant enrichment (P < .001). Blue edges indicate enrichments with in vivo ETS-positive versus negative prostate cancer signatures. (d) Chromatin immunoprecipitation identifies PLAT and PLAU as direct targets of ERG in VCaP cells, by enrichment of ERG binding to the proximal promoters of PLAT and PLAU compared to IgG control. The promoter of KIAA0089 was used as a negative control. (e) VCaP cells were treated with the indicated inhibitors (as in Figure 2g) and assessed for invasion. (f) VCaP cells were treated with transfection reagent alone (untreated), or transfected with nontargeting, PLAU or PLAT siRNA as indicated and assayed for invasion. For all invasion assays, mean (n = 3) ± SEM are shown; *P < .05.