Linc-pint inhibits early stage pancreatic ductal adenocarcinoma growth through TGF-β pathway activation.

Abstract

Long intergenic non-protein coding RNA, p53 induced transcript (Linc-pint) is a newly identified long non-coding RNA, which has demonstrated antitumor activities in various types of cancer. The present study aimed to investigate the role of Linc-pint in pancreatic ductal adenocarcinoma (PDAC). Plasma samples from patients with PDAC, and PDAC and normal cell lines were used in the study. Gene expression was analyzed by reverse transcription-quantitative polymerase chain reaction. Western blotting was used to assess protein level. Transforming growth factor β1 (TGF-β1) plasma level was determined by ELISA. Cancer cell proliferation was measured in vitro with the Cell Counting Kit-8 assy. The results demonstrated that Linc-pint plasma levels were significantly lower in patients with stage 0–1 PDAC compared with healthy controls. In addition, Linc-pint downregulation effectively distinguished patients with PDAC from healthy controls. Linc-pint and TGF-β1 plasma levels were positively correlated in patients with PDAC but not in healthy controls. Furthermore, Linc-pint overexpression upregulated TGF-β1 expression in PDAC cells but not in normal pancreatic ductal cells; however, exogenous TGF-β1 exhibited no significant effects on Linc-pint expression. Linc-pint overexpression and TGF-β1 both inhibited PDAC cell proliferation, whereas treatment with a TGF-β inhibitor reduced their inhibitory effects on cell proliferation. In conclusion, results from the present study suggested that Linc-pint may inhibit early stage PDAC growth through TGF-β pathway activation.