Evidence map›Paper›PMID 30862883›Full record

ArticleScientific reports2019

TRPM2 ion channel promotes gastric cancer migration, invasion and tumor growth through the AKT signaling pathway.

Shekoufeh Almasi, Andra M Sterea, Wasundara Fernando, Derek R Clements, Paola Marcato, David W Hoskin, Shashi Gujar, Yassine El Hiani

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 73 citations in OpenAlex.

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  16. TRPM2-mediated CaCell communication and signaling : CCS · 2023
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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 2 institutions in 2 countries.

Shekoufeh AlmasiDepartments of Biology, Dalhousie University, Halifax, Nova Scotia, B3H 4R2, Canada.
Andra M StereaDepartments of Physiology, and Biophysics, Dalhousie University, Halifax, Nova Scotia, B3H 4R2, Canada.
Wasundara FernandoDepartment of Microbiology and Immunology, Stanford University, Stanford, California, 94305, USA.
Derek R ClementsDepartments of Pathology, Dalhousie University, Halifax, Nova Scotia, B3H 4R2, Canada.
Paola MarcatoDepartment of Microbiology and Immunology, Stanford University, Stanford, California, 94305, USA.
David W HoskinDepartment of Microbiology and Immunology, Stanford University, Stanford, California, 94305, USA.
Shashi GujarDepartment of Microbiology and Immunology, Stanford University, Stanford, California, 94305, USA.
Yassine El HianiDepartments of Physiology, and Biophysics, Dalhousie University, Halifax, Nova Scotia, B3H 4R2, Canada. yassine.elhiani@dal.ca.ORCID 0000-0002-1251-5066
Dalhousie University · CAStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transient Receptor Potential Melastatin-2 (TRPM2) ion channel is emerging as a great therapeutic target in many types of cancer, including gastric cancer - a major health threat of cancer related-death worldwide. Our previous study demonstrated the critical role of TRPM2 in gastric cancer cells bioenergetics and survival; however, its role in gastric cancer metastasis, the major cause of patient death, remains unknown. Here, using molecular and functional assays, we demonstrate that TRPM2 downregulation significantly inhibits the migration and invasion abilities of gastric cancer cells, with a significant reversion in the expression level of metastatic markers. These effects were concomitant with decreased Akt and increased PTEN activities. Finally, TRPM2 silencing resulted in deregulation of metastatic markers and abolished the tumor growth ability of AGS gastric cancer cells in NOD/SCID mice. Taken together, our results provide compelling evidence on the important function of TRPM2 in the modulation of gastric cancer cell invasion likely through controlling the PTEN/Akt pathway.

Indexed as

Cell MovementSignal TransductionAnimalsCalciumCarcinogenesisCell Line, TumorCell ProliferationCytosolDown-RegulationEnzyme ActivationEpithelial-Mesenchymal TransitionGene SilencingHEK293 CellsHumansMaleMice, Inbred NODCalciumProto-Oncogene Proteins c-aktTRPM2 protein, humanTRPM Cation Channels

Identifiers

PMID30862883
PMCPMC6414629
OpenAlexW2921875038

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.