Effects of Long Non-coding RNA Plasmacytoma Variant Translocation 1 Gene on Inflammatory Response and Cell Migration in Infected Gastric Epithelial Cell Line.
10.3881/j.issn.1000-503X.11395
- Author:
Xiao-Hui JING
1
;
Ling-Xue LI
1
;
Tao-Tao HAN
1
;
Juan SHI
1
Author Information
1. National Laboratory of Medical Molecular Biology,Institute of Basic Medical Sciences, CAMS and PUMC,Beijing 100005,China.
- Publication Type:Journal Article
- Keywords:
gastric cancer;
helicobacter pylori;
inflammation-related factors;
long non-coding RNA;
plasmacytoma variant translocation 1
- MeSH:
Cell Line, Tumor;
Cell Movement;
Cytokines;
metabolism;
Epithelial Cells;
cytology;
microbiology;
Gene Knockdown Techniques;
Helicobacter Infections;
pathology;
Helicobacter pylori;
Humans;
Inflammation;
RNA, Long Noncoding;
genetics
- From:
Acta Academiae Medicinae Sinicae
2020;42(2):228-235
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the mechanism of long non-coding RNA plasmacytoma variant translocation 1 (PVT1) in gastric cancer caused by (HP) infection. The expression of PVT1 was detected by quantitative real-time polymerase chain reaction in HP-infected normal gastric epithelial cells GES-1. Gastric cancer cell line SGC-7901 was transfected with PVT1 small interfering RNA and co-cultured with HP,and then the inflammatory cytokines such as tumor necrosis factor-α (TNF-α),interleukin (IL) -1β,IL-6 and IL-8 were detected. After PVT1 was knocked down,the effects of PVT1 on the proliferation and migration of gastric cancer cells were examined by cell scratch assay. RNA-pulldown combined with mass spectrometry was used to detect the protein binding to PVT1,and the result of mass spectrometry was verified by RNA-pulldown combined with Western blot. In HP-infected normal gastric epithelial cells GES-1,quantitative real-time polymerase chain reaction showed that PVT1 was significantly up-regulated (=7.160,=0.019). PVT1 was knocked down in gastric cancer cells,and then infected with HP. The expressions of inflammatory factors including TNF-α (=3.899,=0.011),IL-1β (=14.610,=0.000),and IL-8 (=6.557,=0.001) were significantly inhibited. Although PVT1 knockdown had no significant effect on the proliferation ability of gastric cancer cells,it inhibited the migration of cells. PVT1 might interact with RPS8 protein. PVT1 may act as a pro-inflammatory factor and regulate gastric cancer caused by HP infection.
