Format

Send to

Choose Destination
Saudi J Gastroenterol. 2019 Jan 4. doi: 10.4103/sjg.SJG_309_18. [Epub ahead of print]

Helicobacter pylori DNA promotes cellular proliferation, migration, and invasion of gastric cancer by activating toll-like receptor 9.

Author information

1
Department of Gastroenterology, Changzhou No. 2 People's Hospital, Changzhou, China.
2
Department of Gynecology, Changzhou No. 2 People's Hospital, Changzhou, China.

Abstract

Background/Aim:

Helicobacter pylori (H. pylori) infection is a well-known risk factor for gastric cancer. Toll-like receptor 9 (TLR9) plays an important role in many cancers and is important for immunity to H. pylori infection. Thus, the present study aimed to evaluate the influence of H. pylori on TLR9 and explore its roles in gastric cancer.

Materials and Methods:

TLR9 expression in MKN45 cells, which were cocultured with or without H. pylori or H. pylori DNA, was detected using quantitative reverse transcription-polymerase chain reaction and Western blot assays. Then, TLR9 was knocked down through RNA interference technology in MKN45 cells. Cell Counting Kit-8 assay was performed to investigate cell proliferation, and the Transwell system was established to test the migrative and invasive abilities of MKN45 cells.

Results:

H. pylori infection or H. pylori DNA level was positively correlated with TLR9 upregulation in MKN45 cells. In vitro, H. pylori DNA significantly accelerated cell proliferation and promoted the migration and invasion in MKN45 cells. In contrast, the knockdown of TLR9 significantly suppressed cell proliferation and inhibited the migration and invasion in MKN45 cells.

Conclusions:

The present results suggest that the H. pylori DNA/TLR9-signaling pathway plays an important role in gastric cancer, which might be a potential therapeutic target.

KEYWORDS:

Gastric cancer; H. pylori; invasion; proliferation; toll-like receptor 9

PMID:
30618438
DOI:
10.4103/sjg.SJG_309_18
Free full text

Supplemental Content

Full text links

Icon for Medknow Publications and Media Pvt Ltd
Loading ...
Support Center