Helicobacter pylori CagA oncoprotein interacts with SHIP2 to increase its delivery into gastric epithelial cells.


Journal

Cancer science
ISSN: 1349-7006
Titre abrégé: Cancer Sci
Pays: England
ID NLM: 101168776

Informations de publication

Date de publication:
May 2020
Historique:
received: 20 11 2019
revised: 11 03 2020
accepted: 12 03 2020
pubmed: 22 3 2020
medline: 2 6 2020
entrez: 22 3 2020
Statut: ppublish

Résumé

Chronic infection with Helicobacter pylori cagA-positive strains is causally associated with the development of gastric diseases, most notably gastric cancer. The cagA-encoded CagA protein, which is injected into gastric epithelial cells by bacterial type IV secretion, undergoes tyrosine phosphorylation at the Glu-Pro-Ile-Tyr-Ala (EPIYA) segments (EPIYA-A, EPIYA-B, EPIYA-C, and EPIYA-D), which are present in various numbers and combinations in its C-terminal polymorphic region, thereby enabling CagA to promiscuously interact with SH2 domain-containing host cell proteins, including the prooncogenic SH2 domain-containing protein tyrosine phosphatase 2 (SHP2). Perturbation of host protein functions by aberrant complex formation with CagA has been considered to contribute to the development of gastric cancer. Here we show that SHIP2, an SH2 domain-containing phosphatidylinositol 5'-phosphatase, is a hitherto undiscovered CagA-binding host protein. Similar to SHP2, SHIP2 binds to the Western CagA-specific EPIYA-C segment or East Asian CagA-specific EPIYA-D segment through the SH2 domain in a tyrosine phosphorylation-dependent manner. In contrast to the case of SHP2, however, SHIP2 binds more strongly to EPIYA-C than to EPIYA-D. Interaction with CagA tethers SHIP2 to the plasma membrane, where it mediates production of phosphatidylinositol 3,4-diphosphate [PI(3,4)P

Identifiants

pubmed: 32198795
doi: 10.1111/cas.14391
pmc: PMC7226221
doi:

Substances chimiques

Antigens, Bacterial 0
Bacterial Proteins 0
Phosphatidylinositol Phosphates 0
cagA protein, Helicobacter pylori 0
phosphatidylinositol 3,4-diphosphate 0
PTPN11 protein, human EC 3.1.3.48
Protein Tyrosine Phosphatase, Non-Receptor Type 11 EC 3.1.3.48
INPPL1 protein, human EC 3.1.3.86
Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases EC 3.1.3.86

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1596-1606

Subventions

Organisme : Japan Society for the Promotion of Science
ID : JP16H06373
Organisme : Japan Society for the Promotion of Science
ID : JP19K08436
Organisme : Max-Planck-Gesellschaft

Informations de copyright

© 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

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Auteurs

Yumiko Fujii (Y)

Division of Microbiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Max-Planck Center for Integrative Inflammology, The University of Tokyo, Tokyo, Japan.
Division of Tumor Pathology, Asahikawa Medical University, Asahikawa, Japan.

Naoko Murata-Kamiya (N)

Division of Microbiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.

Masanori Hatakeyama (M)

Division of Microbiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Max-Planck Center for Integrative Inflammology, The University of Tokyo, Tokyo, Japan.

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Classifications MeSH