Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
  • Clinical Research and Public Health
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Video Abstracts
  • Reviews
    • View all reviews ...
    • Complement Biology and Therapeutics (May 2025)
    • Evolving insights into MASLD and MASH pathogenesis and treatment (Apr 2025)
    • Microbiome in Health and Disease (Feb 2025)
    • Substance Use Disorders (Oct 2024)
    • Clonal Hematopoiesis (Oct 2024)
    • Sex Differences in Medicine (Sep 2024)
    • Vascular Malformations (Apr 2024)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Clinical Research and Public Health
    • Research Letters
    • Letters to the Editor
    • Editorials
    • Commentaries
    • Editor's notes
    • Reviews
    • Viewpoints
    • 100th anniversary
    • Top read articles

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Video Abstracts
  • In-Press Preview
  • Clinical Research and Public Health
  • Research Letters
  • Letters to the Editor
  • Editorials
  • Commentaries
  • Editor's notes
  • Reviews
  • Viewpoints
  • 100th anniversary
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
H. pylori infection alters repair of DNA double-strand breaks via SNHG17
Taotao Han, … , Jiazeng Sun, Juan Shi
Taotao Han, … , Jiazeng Sun, Juan Shi
Published June 15, 2020
Citation Information: J Clin Invest. 2020;130(7):3901-3918. https://doi.org/10.1172/JCI125581.
View: Text | PDF
Research Article Gastroenterology Oncology Article has an altmetric score of 4

H. pylori infection alters repair of DNA double-strand breaks via SNHG17

  • Text
  • PDF
Abstract

Chronic infections can lead to carcinogenesis through inflammation-related mechanisms. Chronic infection of the human gastric mucosa with Helicobacter pylori is a well-known risk factor for gastric cancer. However, the mechanisms underlying H. pylori–induced gastric carcinogenesis are incompletely defined. We aimed to screen and clarify the functions of long noncoding RNAs (lncRNAs) that are differentially expressed in H. pylori–related gastric cancer. We found that lncRNA SNHG17 was upregulated by H. pylori infection and markedly increased the levels of double-strand breaks (DSBs). SNHG17 overexpression correlated with poor overall survival in patients with gastric cancer. The recruitment of NONO by overabundant nuclear SNHG17, along with the role of cytoplasmic SNHG17 as a decoy for miR-3909, which regulates Rad51 expression, shifted the DSB repair balance from homologous recombination toward nonhomologous end joining. Notably, during chronic H. pylori infection, SNHG17 knockdown inhibited chromosomal aberrations. Our findings suggest that spatially independent deregulation of the SNHG17/NONO and SNHG17/miR-3909/RING1/Rad51 pathways upon H. pylori infection promotes tumorigenesis in gastric cancer by altering the DNA repair system, which is critical for the maintenance of genomic stability. Upregulation of SNHG17 by H. pylori infection might be an undefined link between cancer and inflammation.

Authors

Taotao Han, Xiaohui Jing, Jiayu Bao, Lianmei Zhao, Aidong Zhang, Renling Miao, Hui Guo, Baoguo Zhou, Shang Zhang, Jiazeng Sun, Juan Shi

×

Figure 7

Nuclear SNHG17 directly interacts with NONO.

Options: View larger image (or click on image) Download as PowerPoint
Nuclear SNHG17 directly interacts with NONO.
(A) RNA pull-down analysis ...
(A) RNA pull-down analysis of the binding of SNHG17 with NONO in total protein extracted from SGC-7901 cells infected with H. pylori. Samples were assayed 3 times. (B) NONO UV-RIP or native RIP followed by qPCR analysis of copurified RNA in SGC-7901 cells with H. pylori infection. Data are represented as mean ± SEM. n = 3. *P < 0.05, 2-tailed Student’s t test. (C) RNA pull-down analysis of the binding of SNHG17 with NONO in SGC-7901 cells infected with or without H. pylori. Samples were assayed 3 times. (D) Confocal microscopy images of SNHG17 stained with FISH probe (red) combined with immunofluorescence analysis of endogenous NONO (green) in SGC-7901 cells upon H. pylori infection. Nuclei were stained with DAPI (blue). Scale bar: 10 μm. Experiments were performed 3 times.

Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts

Posted by 7 X users
45 readers on Mendeley
See more details