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Retinoic acid-related Orphan Receptor alpha (RORα; NR1F1) is a widely distributed nuclear receptor involved in several (patho)physiological functions including lipid metabolism, inflammation, angiogenesis, and circadian rhythm. To better understand the role of this nuclear receptor in liver, we aimed at displaying genes controlled by RORα in liver cells by generating HepG2 human hepatoma cells stably over-expressing RORα. Genes whose expression was altered in these cells versus control cells were displayed using micro-arrays followed by qRT-PCR analysis. Expression of these genes was also altered in cells in which RORα was transiently over-expressed after adenoviral infection. A number of the genes found were involved in known pathways controlled by RORα, for instance  LPA ,  NR1D2  and  ADIPOQ  in lipid metabolism,  ADIPOQ  and  PLG  in inflammation,  PLG  in fibrinolysis and  NR1D2  and  NR1D1  in circadian rhythm. This study also revealed that genes such as  G6PC , involved in glucose homeostasis, and  AGRP , involved in the control of body weight, are also controlled by RORα. Lastly,  SPARC , involved in cell growth and adhesion, and associated with liver carcinogenesis, was up-regulated by RORα.  SPARC  was found to be a new putative RORα target gene since it possesses, in its promoter, a functional RORE as evidenced by EMSAs and transfection experiments. Most of the other genes that we found regulated by RORα also contained putative ROREs in their regulatory regions. Chromatin immunoprecipitation (ChIP) confirmed that the ROREs present in the  SPARC ,  PLG ,  G6PC ,  NR1D2  and  AGRP  genes were occupied by RORα in HepG2 cells. Therefore these genes must now be considered as direct RORα targets. Our results open new routes on the roles of RORα in glucose metabolism and carcinogenesis within cells of hepatic origin.

Control of Gene Expression by the Retinoic Acid-Related Orphan Receptor Alpha in HepG2 Human Hepatoma Cells