Suppressive efficiency of RASSF1A in endometrial carcinoma via inhabiting estrogen receptor alpha expression and ERK pathway activation.

INTRODUCTION

Known as a tumor suppressor, the Ras association domain family 1 isoform A (RASSF1A) is implicated in many human cancers, such as endometrial carcinoma. There is little known about the tumor inhibitive effects of RASSF1A on endometrial carcinoma. The present study was designed to investigate the role of RASSF1A in HEC-1-A cells and to explore its potential mechanisms.

MATERIALS AND

METHODS

In this study, overexpression of RASSF1A was established by transfection the recombinant adenoviral RASSF1A in HEC-1-A cells. Cells viability was assessed by MTT assay and the apoptosis was analyzed using flow cytometry. Cell migration and invasion were measured in Transwell assay. The levels of ERα and PELP1 protein and extracellular regulated protein kinase (ERK) pathway activation were detected by Western blot.

RESULTS

RASSF1A over-expression could significantly inhibit the proliferation, migration and invasion of the HEC-1-A cells in transfection with RASSF1A group compared to that in transfection with control group, also induced apoptosis and suppressed the tumor growth after injection in nude mice. Moreover, overexpression of RASSF1A could inhibit the ERK signal pathway activation and decrease the ERα and PELP1 expression.

CONCLUSION

Tumor suppressive efficiency of RASSF1A is exerted through the regulation of ERK pathway activation, ERα and PELP1 expression.