Evidence map›Paper›PMID 28481365›Full record

ArticleOncogenesis2017

Membrane-bound β-catenin degradation is enhanced by ETS2-mediated Siah1 induction in Helicobacter pylori-infected gastric cancer cells.

L Das, S B Kokate, P Dixit, S Rath, N Rout, S P Singh, S E Crowe, A Bhattacharyya

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2017. 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
0.8field-weighted citation impact, top 29% 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, 22 citations in OpenAlex.

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  13. Identification of histone deacetylase 8 as a novel therapeutic target for renal fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
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  14. Review
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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 2 countries.

L DasSchool of Biological Sciences, National Institute of Science Education and Research (NISER) Bhubaneswar, Jatni, Odisha, India.
S B KokateSchool of Biological Sciences, National Institute of Science Education and Research (NISER) Bhubaneswar, Jatni, Odisha, India.
P DixitSchool of Biological Sciences, National Institute of Science Education and Research (NISER) Bhubaneswar, Jatni, Odisha, India.
S RathSchool of Biological Sciences, National Institute of Science Education and Research (NISER) Bhubaneswar, Jatni, Odisha, India.
N RoutDepartment of Oncopathology, Acharya Harihar Regional Cancer Centre, Cuttack, Odisha, India.
S P SinghDepartment of Gastroenterology, SCB Medical College, Cuttack, Odisha, India.
S E CroweSchool of Medicine, Division of Gastroenterology, UC San Diego, California, USA.
A BhattacharyyaSchool of Biological Sciences, National Institute of Science Education and Research (NISER) Bhubaneswar, Jatni, Odisha, India.
National Institute of Science Education and Research · INRegional Cancer Center, Thiruvananthapuram · INSriram Chandra Bhanja Medical College Hospital · INUniversity of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-catenin has two different cellular functions: intercellular adhesion and transcriptional activity. The E3 ubiquitin ligase Siah1 causes ubiquitin-mediated degradation of the cytosolic β-catenin and therefore, impairs nuclear translocation and oncogenic function of β-catenin. However, the effect of Siah1 on the cell membrane bound β-catenin has not been studied. In this study, we identified that the carcinogenic bacterium H. pylori increased ETS2 transcription factor-mediated Siah1 protein expression in gastric cancer cells (GCCs) MKN45, AGS and Kato III. Siah1 protein level was also noticeably higher in gastric adenocarcinoma biopsy samples as compared to non-cancerous gastric epithelia. Siah1 knockdown significantly decreased invasiveness and migration of H. pylori-infected GCCs. Although, Siah1 could not increase degradation of the cytosolic β-catenin and its nuclear translocation, it enhanced degradation of the membrane-bound β-catenin in the infected GCCs. This loss of membrane-bound pool of β-catenin was not associated with the proteasomal degradation of E-cadherin. Thus, this work delineated the role of Siah1 in increasing invasiveness of H. pylori-infected GCCs.

Identifiers

PMID28481365
PMCPMC5523059
OpenAlexW2612303134

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.