Expression of Endoglin in Primary Endometrial Cancer

Abstract

Objective: Alterations in the transforming growth factor-β (TGF-β) signaling cascade are engaged in the development of human neoplasms through the deregulation of proliferation, differentiation and migration. However, in endometrial cancer, the role of endoglin, which acts as an accessory receptor in the TGF-β pathway, is still unknown. The aim of our study was the evaluation of endoglin mRNA and protein expression levels in endometrial cancer as compared to normal endometrium. TGF-β₁ and TGF-β type II receptor were involved in the investigation since they directly cooperate with endoglin during signal propagation. Obtained results were correlated with clinicopathological parameters of studied material to determine endoglin contribution to tumor development and progression. Methods: mRNA level assessment was performed using real-time technique, whereas protein expression was determined by ELISA assay. Results: The endoglin mRNA level was not significantly altered in cancerous samples as compared to normal tissue, whereas its protein level demonstrated significant upregulation (p < 0.001) associated with increased tumor malignancy, assessed by histological grade and myometrium infiltration. Conclusions: An increase in endoglin protein expression level may interfere with the oncogenic potential of TGF-β₁ and TGF-β type II receptor in endometrial cancer. Correlation of the endoglin level with pronounced cancer malignancy suggests that it may be regarded as a potential prognostic marker of primary endometrial cancer.