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. 2014 Dec 8;207(5):627–642. doi: 10.1083/jcb.201405105

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Figure 9. — CDK5 stimulates tumor suppressor activities of DLC1, and is pro-oncogenic when the DLC1 level is reduced. (A) Analysis of a Jacob dataset of 442 human NSCLC cases that were well, moderately, or poorly differentiated. The graph represents the number and percentage of cases in each differentiation category that had both high CDK5 and low DLC1 mRNA expression. (B) Anchorage-independent growth of DLC1-negative H358 cells in the absence and presence of Roscovitine. Roscovitine treatment inhibits colony formation and growth in soft agar. Bar, 2 mm. (C) Quantification of agar colonies (>0.4 mm) in the Roscovitine-treated and untreated group from three independent experiments as shown in B. (D) Anchorage-independent growth of H1703 cells in the absence and presence of DLC1 and with or without Roscovitine treatment. Roscovitine does not inhibit anchorage-independent growth of parental H1703 cells, which express endogenous DLC1, but does inhibit growth when DLC1 expression is knocked down. Bar, 2 mm. (E) Quantification of agar colonies in the presence and absence of DLC1, and with and without Roscovitine treatment. Roscovitine treatment of DLC1-positive H1703 parental cells did not alter the number of soft agar colonies >0.4 mm, but it reduced the number of colonies after siRNA knockdown of endogenous DLC1. n = 3. (F) Knockdown of DLC1 expression by DLC1 siRNA (top). GAPDH was used as a loading control (bottom). Error bars indicate ± SD.