Abstract
Liver X receptors (LXRs) are important sensors and regulators for cholesterol, fatty acid, and glucose and play essential roles in the development and progression of cardiovascular diseases. Liver X receptors (LXRs) belong to the nuclear superfamily and contain two isoforms: LXR and LXR. LXR dimerizes with RXR in response to the stimulation of either one's agonists. We previously reported that treatment with LXR agonists suppresses the tumor growth and the disease progression of prostate cancer. In this study, we examined if treatment with T0901317, the most potent LXR agonist, may suppress angiogenesis. The results of tube formation assay indicated that treatment with T0901317 inhibited the tube formation of HUVEC cells. T0901317 treatment suppressed migration of HUVEC cells as determined by migration assay and inhibited angiogenesis in chorioallantoic membranes assay in vivo. Angiogenesis protein array revealed that T0901317 treatment suppresses inflammation response. Our results suggested that activation of LXR may interfere angiogenesis via induction of inflammation-related proteins and LXR target genes as well as decrease of angiogenesis regulatory proteins. We discovered that Apolipoprotein D (ApoD) may be a potential target for tumor angiogenesis inhibition. Based on our findings, we believe that administration of LXR agonist T0901317 may be a potential treatment for cancer agiogenesis.