Transcriptomic changes in human SCC-25 Parental and RARG knockout cells in response to 6h and 48h treatments with RAR? agonists CD1530 or all-trans retinoic acid (RA).
Vitamin A (retinol) metabolism and signaling through nuclear retinoic acid receptors (RARs a,ß,?) regulate embryonic development, immune functions, and cell differentiation in most cell types.  RAR gamma (RAR?) is highly expressed in stratified squamous epithelial cells of the tongue, esophagus, and skin.  While data indicate that RAR? agonism is anti-tumorigenic in oral cavity squamous cell carcinoma (OCSCC), the specific, primary gene targets of RAR? remain poorly characterized. Here, we define the transcriptomic consequences of RAR? activity in OCSCC. Using a CRISPR-Cas9-mediated knockout (KO) of RAR? and pharmacological treatments with RAR agonists, we identified RAR?-specific gene targets and pathways, as well as targets that overlap with other RA-responsive nuclear receptors. Overall design: RNA-seq profiling of parental SCC-25 cells and their CRISPR-mediated RARG knockout derivative (RARGKO) with and without added ligand (1µM synthetic RAR? agonist CD1530 or 1µM endogeous ligand retinoic acid) at 6h and 48h timepoints.