Abstract
TGFβ signaling cascade plays a vital role in neoplastic transformation, but the function of betaglycan, which is a TGFβ 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 TGFβ canonical signaling components, i.e., TGFβ1, TGFβ2, and TGFβRII, 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 TGFβ2-induced signaling.
Published Version
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