Evidence map›Paper›PMID 26376616›Full record

ArticleOncotarget2015

Phosphorylation and inactivation of PTEN at residues Ser380/Thr382/383 induced by Helicobacter pylori promotes gastric epithelial cell survival through PI3K/Akt pathway.

Zhen Yang, Chuan Xie, Wenting Xu, Gongmeizi Liu, Ximei Cao, Wei Li, Jiang Chen, Yin Zhu, Shiwen Luo, Zhijun Luo and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 55 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

Zhen YangDepartment of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Chuan XieDepartment of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Wenting XuDepartment of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Gongmeizi LiuDepartment of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Ximei CaoDepartment of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Wei LiDepartment of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Jiang ChenDepartment of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Yin ZhuDepartment of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Shiwen LuoDepartment of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Zhijun LuoThe Medical College of Nanchang University, Nanchang, Jiangxi, China.
Nonghua LuDepartment of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
First Affiliated Hospital of Nanchang University · CNNanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phosphorylation of PTEN at residues Ser380/Thr382/383 leads to loss of phosphatase activity and tumor suppressor function. Here, we found that phosphorylation of PTEN at residues Ser380/Thr382/383 was increased with gastric carcinogenesis, and more importantly, Helicobacter pylori was a trigger of this modification in chronic non-atrophic gastritis. H. pylori could phosphorylate and inactivate PTEN in vivo and in vitro, resulting in survival of gastric epithelial cells. Furthermore, stable expression of dominant-negative mutant PTEN or inhibition of Akt prevented the enhanced survival induced by H. pylori. These results indicate that PTEN phosphorylation at residues Ser380/Thr382/383 is a novel mechanism of PTEN inactivation in gastric carcinogenesis, and H. pylori triggers this modification, resulting in activation of the PI3K/Akt pathway and promotion of cell survival.

Indexed as

Cell ProliferationAdenocarcinomaAnimalsApoptosisBlotting, WesternCells, CulturedEpithelial CellsGastric MucosaGastritisGerbillinaeHelicobacter InfectionsHelicobacter pyloriHumansImmunoenzyme TechniquesMalePhosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humangastric carcinogenesisHelicobacter pyloriphosphatase and tensin homologphosphorylationPI3K/Akt pathway

Identifiers

PMID26376616
PMCPMC4741650
OpenAlexW2274643887

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.