Figure 2.

CSNK1E is a target for developing anti-cancer drugs with a potentially high therapeutic index. (a) Retesting of six hit shRNA clones in isogenic BJ-derived cell lines. Knocking down CSNK1E induced cancer-cell-specific growth inhibition, whereas knocking down other survival genes did not display differential activity in the two cell lines. The graph is representative of multiple experiments. (b) The activity of shCSNK1E was examined in four isogenic BJ-derived cell lines. The growth inhibitory effect of shCSNK1E was proportional to the cell proliferation rate. The doubling time of each cell line is shown in parentheses. (c) Inhibition of HT1080 cell growth by independent shRNA clones that bind to different regions of CSNK1E mRNA. (d) The knockdown efficiency of each shRNA clone targeting CSNK1E as assessed by quantitative PCR analysis. Error bars in (b-d) indicate one standard deviation of triplicate data.

Yang and Stockwell Genome Biology 2008 9:R92   doi:10.1186/gb-2008-9-6-r92
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