Evidence map›Paper›PMID 27048589›Full record

ArticleThe Biochemical journal2016

ETS2 and Twist1 promote invasiveness of Helicobacter pylori-infected gastric cancer cells by inducing Siah2.

Lopamudra Das, Shrikant Babanrao Kokate, Suvasmita Rath, Niranjan Rout, Shivaram Prasad Singh, Sheila Eileen Crowe, Asish K Mukhopadhyay, Asima Bhattacharyya

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 28 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

8 authors at 4 institutions in 1 country.

Lopamudra DasSchool of Biological Sciences, National Institute of Science Education and Research (NISER), P.O. Bhimpur-Padanpur, Via Jatni, Dist. Khurda 752050, Odisha, India.
Shrikant Babanrao KokateSchool of Biological Sciences, National Institute of Science Education and Research (NISER), P.O. Bhimpur-Padanpur, Via Jatni, Dist. Khurda 752050, Odisha, India.
Suvasmita RathSchool of Biological Sciences, National Institute of Science Education and Research (NISER), P.O. Bhimpur-Padanpur, Via Jatni, Dist. Khurda 752050, Odisha, India.
Niranjan RoutDepartment of Oncopathology, Acharya Harihar Regional Cancer Centre, Cuttack 753007, Odisha, India.
Shivaram Prasad SinghDepartment of Gastroenterology, SCB Medical College, Cuttack 753007, Odisha, India.
Sheila Eileen CroweSchool of Medicine, Division of Gastroenterology, UC San Diego, CA 92093, U.S.A.
Asish K MukhopadhyayDivision of Bacteriology, National Institute of Cholera and Enteric Diseases (NICED), Kolkata 700010, India.
Asima BhattacharyyaSchool of Biological Sciences, National Institute of Science Education and Research (NISER), P.O. Bhimpur-Padanpur, Via Jatni, Dist. Khurda 752050, Odisha, India asima@niser.ac.in.
National Institute of Science Education and Research · INNational Institute of Cholera and Enteric Diseases · INRegional Cancer Center, Thiruvananthapuram · INSriram Chandra Bhanja Medical College Hospital · IN

Funding

OXIDATIVE INJURY TO GASTRIC EPITHELIAL CELLS BY H. PYLORIR01DK061769 · NIDDK · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI CROWE, SHEILA E. · 2001 to 2015
$3.6M
NIDDK NIH HHS R01 DK061769
6 · The paper itself

Abstract

Helicobacter pylori infection is one of the most potent factors leading to gastric carcinogenesis. The seven in absentia homologue (Siah2) is an E3 ubiquitin ligase which has been implicated in various cancers but its role in H. pylori-mediated gastric carcinogenesis has not been established. We investigated the involvement of Siah2 in gastric cancer metastasis which was assessed by invasiveness and migration of H. pylori-infected gastric epithelial cancer cells. Cultured gastric cancer cells (GCCs) MKN45, AGS and Kato III showed significantly induced expression of Siah2, increased invasiveness and migration after being challenged with the pathogen. Siah2-expressing stable cells showed increased invasiveness and migration after H. pylori infection. Siah2 was transcriptionally activated by E26 transformation-specific sequence 2 (ETS2)- and Twist-related protein 1 (Twist1) induced in H. pylori-infected gastric epithelial cells. These transcription factors dose-dependently enhanced the aggressiveness of infected GCCs. Our data suggested that H. pylori-infected GCCs gained cell motility and invasiveness through Siah2 induction. As gastric cancer biopsy samples also showed highly induced expression of ETS2, Twist1 and Siah2 compared with noncancerous gastric tissue, we surmise that ETS2- and Twist1-mediated Siah2 up-regulation has potential diagnostic and prognostic significance and could be targeted for therapeutic purpose.

Indexed as

Cell Line, TumorEpithelial CellsGastric MucosaHelicobacter InfectionsHelicobacter pyloriHumansIn Vitro TechniquesNuclear ProteinsProtein BindingProto-Oncogene Protein c-ets-2Seven in Absentia ProteinsStomach NeoplasmsTwist-Related Protein 1Ubiquitin-Protein LigasesETS2 protein, humanNuclear ProteinsProto-Oncogene Protein c-ets-2Seven in Absentia ProteinsTWIST1 protein, humanTwist-Related Protein 1Ubiquitin-Protein LigasesETS2gastric cancerH. pylorimetastasisSiah2Twist1

Identifiers

PMID27048589
PMCPMC4888467
OpenAlexW2325682670

What OpenQuestion holds

Textmetadata
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.