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. 2014 Nov 12;5(20):9626–9640. doi: 10.18632/oncotarget.2437

Figure 3. Inhibition of G12 signaling and knockdown of Gα12 in OSCC.

Figure 3

(A) Total protein levels of Gα12 and Gα13 were not affected in ORL48 cells transduced with GFP-fused RGS chimeric molecule. (B) Endogenous levels of activated RhoA were reduced in ORL48/RGS cells and remained inhibited even up to 10 minutes post LPA and thrombin stimulation, as compared to the ORL48/GFP control. (C) In scratch assays, the expression of GFP-fused RGS chimeric molecule in ORL48 consistently inhibited cell migration, as indicated by a significant larger open wound area compared to the ORL48/GFP control cells after 18 hours. (D) The expression of Gα12 in ORL48 which endogenously expresses high levels of Gα12 was knockdown using 2 separate shRNA sequences for Gα12 as shown by western blot. (E) Gα12 knockdown in ORL48 by shRNA inhibited OSCC cell migration and invasion in the transwell assays. ORL48/shGα12 cells showed a significant reduction in cell migration and invasion when tested with 2 different chemoattractant (NIH3T3 conditioned medium and 1U/ml thrombin). The graphs are the representative results of 3 experimental repeats. Error bars represent SEM for the replicates tested in an experiment.