Objective Several studies have reported that retinoic acid (RA) might be used to treat malignancies. The effects of RA are mediated by the RA receptor (RAR), and RAR/RAR especially acts as a tumor suppressor. However, little is known about its role in human endometrial cancer. Materials and Methods In this study, we examined the effects of all-trans RA (ATRA) on progression of human endometrial cancer cell line, RL95-2 and Hec1A. We then examined the expression of RAR and RAR in 50 endometrial cancer tissues by using immunohistochemistry. Results We found inhibitory effects of ATRA on cell proliferation, apoptosis, and migration in RL95-2 cells, but not in Hec1A cells. RAR or RAR knockdown individually could not cancel out the inhibition of cell proliferation by ATRA in RL95-2 cells, but simultaneous knockdown of RAR and RAR could block its effect on proliferation. RAR and RAR knockdown dose dependently reduced the inhibition of migration by ATRA, but the effect was more pronounced with RAR knockdown than with RAR knockdown. We confirmed that RAR gene was directly regulated by ATRA in microarray and real-time reverse transcription polymerase chain reaction. Furthermore, the RAR agonist (BMS453) significantly suppressed proliferation of RL95-2 cells. In immunohistochemical analysis, RAR expression was positively correlated with tumor grade, and RAR showed the opposite tendency in endometrial cancer. Conclusions Retinoic acid might have multiple antitumor effects, and RAR may be a potent therapeutic target in RA treatment for endometrial cancers.