Fig. 9.
A. Anti-GRM1 siRNA constructs introduced into UOK117 RCC cells permitted doxycycline-inducible knockdown of endogenous GRM1 at the protein level as assessed by immunoblots. GRM1 + control is IMR32 cell extract. Levels of GRM1 expression in three independent siGRM1-UOK117 clones as percentage of control Day 0, by densitometry.
B. In vivo reduction of tumor progression by anti-GRM1 siRNA. Mice bearing xenografted tumors developing from two independent clones of siGRM1-UOK117 RCC cells chosen from Fig. 9a were treated with doxycycline to induce siRNA knockdown of endogenous GRM1 levels. Results implied sustained expression of GRM1 is in part necessary to maintain UOK117 tumor progression (both clones P < 0.001, t test, n=20).