Dysregulation of betaglycan expression in primary human endometrial carcinomas.

TGFß signaling cascade plays a vital role in neoplastic transformation, but the function of betaglycan, which is a TGFß accessory receptor, is still unknown in particular cancer. Evaluation of betaglycan expression both at mRNA (real-time PCR) and protein (ELISA) level in the context of TGFß canonical signaling components, i.e., TGFß1, TGFß2, and TGFßRII, in endometrial carcinomas was performed. Betaglycan mRNA expression level was significantly (p < .001) downregulated with simultaneous betaglycan protein level upregulation in cancer samples. Obtained results suggest that endometrial cancer is associated with disruption of accessory receptor betaglycan expression, what may alter TGFß2-induced signaling.