Figure 5.

Validation of CSMA screening results. (A) Comparison of the mean z-score of Ki-67/cPARP index of all analyzed cell lines with clinical gene expression levels of GPCRs in clinical prostate cancer samples (n = 349) vs. healthy prostate samples (n = 147) webcite. (B) Unsupervised hierarchical clustering of the averaged siRNA z-scores for the top 5 highest ranking candidate genes identified on basis of rank product analysis of common impact on all the cell types (Top) and on basis of prostate cancer cell line specific growth inhibitory impact (Bottom). (C) Representative x20 microscope images of the GPR160 (siRNA Q024145) CSMA spots for RWPE-1, LAPC-4 and VCaP cells. Scale bar100 μm. (D) Comparison of mRNA transcript levels of GPR160 and NPY in a panel of commonly used prostate model cell lines. Log2 Affymetrix scale. (E) An enzymatic cell viability assay was used to verify the Ki-67/cPARP based growth inhibitory effect of GPR160 and NPY in VCaP, LAPC-4, 22Rv1, RWPE-1 and PC3 cells. ** p < .01, * p < .05.

Rantala et al. BMC Genomics 2011 12:162   doi:10.1186/1471-2164-12-162
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