No abstract

As one of the most aggressive types of tumor, pancreatic cancer is a principal cause of tumor-associated mortality. Negative associations between microRNA-29 (miR-29) and DNA methyltransferases (DNMT) 3a and 3b have been demonstrated to be associated with the carcinogenesis of a number of types of cancer; however, this has not been completely elucidated in pancreatic cancer. In the present study, pancreatic cancer tissues (n=15) and corresponding paracancerous tissues (n=15) were obtained and the results of reverse transcription-quantitative polymerase chain reaction analysis indicated decreased expression of miR-29b and enhanced mRNA expression of DNMT3b in pancreatic cancer tissues, compared with the corresponding paracancerous tissues. Increased protein expression of DNMT3b was demonstrated by western blotting and immunohistochemistry. In addition, the negative association between miR-29b and DNMT3b was noted in pancreatic cancer tissues, and luciferase reporter assays confirmed that miR-29b was able to directly target DNMT3b in vitro. Notably, miR-29b overexpression was able to decrease cell viability and to promote the apoptosis by targeting DNMT3b, and the knockdown of DNMT3b exhibited consistent results in vitro and in vivo. The results of the present study suggested that miR-29b, as a tumor suppressor, may be a novel target for the development of treatments for pancreatic cancer.

Activated rat HSCs lower the Th1/Th2 profile, inhibiting the Th1 response and enhancing the Th2 response, and this may be a novel pathway for liver fibrogenesis.