Identification of new molecular targets for the treatment of endometrial cancer (EC) is an important clinical goal, especially for the patients which were resistant to conventional therapies. The aryl hydrocarbon receptor (AhR) is a ligand- activated transcription factor known primarily as the mediator of dioxin toxicity. However, the AhR can also inhibit cellular proliferation in a ligand-dependent manner and act as a tumor suppressor in mice, thus may be a potential anticancer target. In this study, we investigated if the endogenous AhR ligand 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) regulated proliferation and migration of EC cells via AhR. We used quantitative real-time PCR and western blot to assess the expression of AhR in EC tissues and paired adjacent normal tissues. In addition, we conducted transwell assay to test whether the treatment of ITE altered the locomotive potential and proliferation of EC cells. Next, we conducted mouse xenograft models to further explore the in vivo effect of ITE. We found that the AhR protein and RNA levels were increased mildly in EC tissues relative to the para-tumor normal endometrial tissues. Besides, ITE suppressed EC cells proliferation and migration in vitro, and also suppressed EC cells xenograft growth in mice. Our results strongly supported the possibility of using the ITE as a small molecular compound for the treatment of EC.