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. Author manuscript; available in PMC: 2010 Feb 15.
Published in final edited form as: Cancer Res. 2009 Feb 10;69(4):1536–1544. doi: 10.1158/0008-5472.CAN-08-3718

Figure 2. Changes in morphology and induction of RhoB is PPARγ-dependent.

Figure 2

A. Live microscopic images of KTC2 and KTC3 cell lines treated with and without 10 nM RS5444 for 24 hrs at 40X magnification revealed altered morphology. Real Time PCR for multiple RhoGTPases in cell lines treated with RS5444 for 24 hrs demonstrated an increase of RhoB mRNA with no appreciable alteration in mRNA levels of the other RhoGTPases. Experiments were performed in triplicate. * indicates p<0.05 when compared to untreated control. B. Three Tzd PPARγ agonists (10 nM RS5444, 100 nM rosiglitazone, 1 μM troglitazone) induced RhoB protein expression in DRO and KTC2 cells examined 24 hrs after treatment. When the irreversible PPARγ antagonist, GW9662, was added 5 min prior to Tzd treatment, induction of RhoB was blocked demonstrating specificity for PPARγ. C. Western analysis of lentiviral infected DRO and KTC2 cells silenced for PPARγ illustrates a lack of RhoB upregulation in the absence of PPARγ when treated with RS5444. D. Western analysis demonstrated induction of RhoB expression in tumors (DRO, ARO and THJ-11T) grown in athymic nude mice following chronic oral treatment (4 weeks) with 0.025% RS5444 versus that of vehicle control. Results from three random animals of each group are shown.