Open AccessLong non‑coding RNA lnc‑GNAT1‑1 inhibits gastric cancer cell proliferation and invasion through the Wnt/β‑catenin pathway in Helicobacter�pylori infection
Author(s) -
Liping Liu,
Tiankui Shuai,
Bin Li,
Lei Zhu,
Xun Li
Publication year - 2018
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2018.9405
Subject(s) - oncogene , biology , wnt signaling pathway , cancer research , cancer , cell cycle , helicobacter pylori , cell growth , cancer cell , transfection , catenin , microbiology and biotechnology , signal transduction , cell culture , genetics
The aim of the present study was to investigate the effect of long non‑coding (lnc)‑G protein subunit α transducin 1 (GNAT1)‑1 in gastric cancer cells infected with Helicobacter (H.) pylori. Reverse transcription‑quantitative polymerase chain reaction was used to assess lnc‑GNAT1‑1 expression in normal gastric and gastric cancer cells infected with H. pylori. The overexpression of lnc‑GNAT1‑1 in SGC‑7901 and MNK45 cells was induced by transfection. Migration and invasion assays were performed in transfected gastric cancer cells to evaluate the effect of lnc‑GNAT1‑1. Histological and western blot analyses were used to determine the alterations in the Wnt/β‑catenin signaling pathway protein expression. Cells transfected with lnc‑GNAT1‑1 were used to initiate gastric cancer tumor xenografts to compare tumor growth in mice inoculated with untransfected cells. The results revealed that H. pylori infection significantly downregulated lnc‑GNAT‑1 expression. Lnc‑GNAT1‑1 overexpression inhibited gastric cancer cell migration and invasion. Wnt/β‑catenin pathway protein expression was decreased by lnc‑GNAT1‑1 overexpression. In addition, lnc‑GNAT1‑1 overexpression reduced tumor growth. Thus, lnc‑GNAT1‑1 is downregulated in gastric cancer infected with H. pylori and lnc‑GNAT1‑1 overexpression inhibited gastric cancer growth through the Wnt/β‑catenin signaling pathway.