Objective: To explore the relationships between Smad4, TGF beta1 and TbetaR II in the TGF-beta pathway and the possible mechanisms by which they effect pancreatic carcinoma.
Methods: The expression of Smad4, TGF beta1 and TbetaR II in paraffin embedded pancreatic carcinoma tissues was detected by using antibodies against Smad4, TGF beta1 and TbetaR II with EnVision immunohistochemistry.
Results: The positive rates of Smad4, TGF beta1 and TbetaR II were 58.93% (33), 66.07% (37) and 60.71% (34), respectively. The positive rates of the above three proteins in matched normal pancreatic tissues were 89.29% (50), 25.00% (14) and 25.00% (14) respectively. There was a significant relationship between the expression of TGF beta1, clinical stage and the metastasis of the tumor (P < 0.05). There was also a significant relationship between the expressions of TGF beta1 and TbetaR II (P < 0.05).
Conclusions: The expression of Smad4 in pancreatic carcinoma tissue is significantly decreased but the expression of TGF beta1 and TbetaR II are increased. Smad4 may play an important role in the regulation of TGFbeta inducible gene expression and subsequent growth inhibition, but TGFbeta may also act in a Smad4-independent manner.