p53 is a mediator for radiation-repressed human TR2 orphan receptor expression in MCF-7 cells, a new pathway from tumor suppressor to member of the steroid receptor superfamily

Abstract

p53 may function as a checkpoint by arresting the G1 cell cycle in response to DNA damage induced by radiation or other stimuli. We have found that the expression of the TR2 orphan receptor (TR2), a member of the steroid receptor superfamily, was down-regulated by ionizing irradiation. Our data shown in the present study demonstrate that irradiation can repress TR2 at both the translational and transcriptional levels. Transient transfection assays further link p53 to this repression by proving that endogenously induced or exogenously transfected p53 can repress TR2 gene expression, and this repression can be reversed by the co-transfection of SV40 large T antigen. Together, our data demonstrate for the first time that radiation and p53 can repress TR2, possibly providing a new pathway to link ionizing irradiation and p53 to members of the steroid receptor superfamily.