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.