Overexpression of p16(ink4a) regulates the Wnt/beta-catenin signaling pathway in pancreatic cancer cells

摘要

The pathogenesis and etiology of pancreatic cancer remain to be fully elucidated; therefore, associated investigations are required to improve the outcome and prognosis of patients. In the present study, the effects of the overexpression of p16(ink4a) on the Wnt/beta-catenin signaling pathway were investigated in pancreatic cancer cell lines. Two pancreatic cancer cell lines, Bxpc-3 and Miapaca-2, characterized by low expression of p16(ink4a), were transfected with the pc-DNA3.0-p(16ink4a) plasmid. After 24 h, Reverse transcription-polymerase chain reaction and western blot analyses were performed to evaluate the expression of p16(ink4a), beta-catenin, which is a key molecule in the Wnt/beta-catenin signaling pathway, c-myc and cyclin D1, which are molecules downstream of beta-catenin. The expression of p16(ink4a) was significantly upregulated in the transfected cells. Consequently, the expression of beta-catenin was inhibited, whereas the expression levels of c-myc and cyclin D1 were not altered significantly. The increased expression of p16(ink4a) may affect the activity of Wnt/beta-catenin signaling through modulation of the expression of beta-catenin. The results of the present study provide information for the future development of targeted treatments for pancreatic cancer.