Artemin Stimulates Oncogenicity and Invasiveness of Endometrial Carcinoma Cells

摘要

Here, we provide evidence for a functional role of artemin (ARTN) in progression of endometrial carcinoma (EC). Increased ARTN protein expression was observed in EC,and ARTN protein expression in EC was significantly associated with higher tumor grade and invasiveness. Forced expression of ARTN in EC cells significantly increasedtotal cell number as a result of enhanced cell cycle progression and cell survival. In addition, forced expression of ARTN significantly enhanced anchorage-independentgrowth and invasiveness of EC cells. Moreover, forced expression of ARTN increased tumor size in xenograft models and produced highly proliferative, poorly differ-entiated,andinvasivetumors.TheARTN-stimulatedincreasesinoncogenicityandinvasionweremediatedbyincreasedexpressionandactivityofAKT1.SmallinterferingRNA-mediated depletion or antibody inhibition of ARTN significantly reduced oncogenicity and invasion of EC cells. Thus, inhibition of ARTN may be considered as apotential therapeutic strategy to retard progression of EC.