Aryl hydrocarbon receptor exogenous ligand 3-methylchoranthrene inhibited endometrial cancer cells proliferation.

OBJECTIVE

Endometrial cancer (EC) is the most prevalent gynecologic malignancy among women worldwide. Increasing evidence has disclosed the potential role of aryl hydrocarbon receptor (AhR) in the cancer development; however, little is known about its roles in the EC development. In the present study, we evaluated AhR expression in EC tissues as well as cell lines, and investigated the effects of AhR knockdown and exogenous ligand 3-methylchoranthrene (3-MC) on EC cells proliferation and invasion using Ishikawa and ECC-1 cells lines.

MATERIALS AND METHODS

In this study, tissue microarray and immunohistochemistry were used to investigate the expression and localization of AhR in EC tissues. RT-PCR and Western blot were performed to detect the AhR expression. AhR specific siRNA was used to knockdown the AhR expression. MTT and transwell assay were carried out to study the EC cells proliferation and invasion, respectively.

RESULTS

Our results showed that AhR was highly expressed in the EC tissues and cell lines when compared with its expression in the normal endometrial tissues. AhR siRNA significantly decreased (p < 0.05) AhR protein expression in both Ishikawa and ECC-1 cells. Knockdown of AhR did not alter EC cells proliferation and invasion. However, 3-MC dose-dependently inhibited (p < 0.05) EC cells proliferation via AhR-mediated pathway.

CONCLUSIONS

The results from the current application will provide critical information on roles of 3-MC/AhR pathway in mediating EC growth, which could be useful for future therapeutic intervention in this lethal human disease.