Evidence map›Paper›PMID 32099405›Full record

ArticleOncoTargets and therapy2020

Foretinib Inhibits Cancer Stemness and Gastric Cancer Cell Proliferation by Decreasing CD44 and c-MET Signaling.

Sung-Hwa Sohn, Bohyun Kim, Hee Jung Sul, Bo Youn Choi, Hyeong Su Kim, Dae Young Zang

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

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  7. Receptor tyrosine kinase inhibitors in cancer.Cellular and molecular life sciences : CMLS · 2023
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  17. Antitumor Drugs and Their Targets.Molecules (Basel, Switzerland) · 2020
    Review
  18. Journal of experimental pharmacology · 2020
    Review
  19. Article
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

6 authors at 2 institutions in 1 country.

Sung-Hwa Sohn *Hallym Translational Research Institute, Hallym University Sacred Heart Hospital, Anyang 14066, Republic of Korea.
Bohyun Kim *Hallym Translational Research Institute, Hallym University Sacred Heart Hospital, Anyang 14066, Republic of Korea.
Hee Jung SulHallym Translational Research Institute, Hallym University Sacred Heart Hospital, Anyang 14066, Republic of Korea.
Bo Youn ChoiHallym Translational Research Institute, Hallym University Sacred Heart Hospital, Anyang 14066, Republic of Korea.
Hyeong Su KimDepartment of Internal Medicine, Hallym University Medical Center, Hallym University College of Medicine, Anyang-si, Gyeonggi-do 14068, Republic of Korea.
Dae Young ZangHallym Translational Research Institute, Hallym University Sacred Heart Hospital, Anyang 14066, Republic of Korea.
Hallym University Sacred Heart Hospital · KRHallym University Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeCD44 isoforms are highly expressed in cancer stem cells, initiating tumor growth and sustaining tumor self-renewal. Among these isoforms, CD44 variant 9 (CD44v9) is overexpressed in chronic inflammation-induced cancer. CD44 and the mesenchymal-to-epithelial transition (MET) receptor tyrosine kinase are coactivated in some gastric cancers (GCs). In this study, we characterized MET and CD44 expression and signaling in human GC cell lines and analyzed differences in the susceptibility of these lines to foretinib. PATIENTS AND

methodsWe analyzed cell viability and the rate of apoptotic cells using MTS assays and flow cytometry, respectively. Gene and protein expression were assessed by quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and immunoblotting, respectively.

resultsForetinib treatment resulted in dose-dependent inhibition of growth in c-MET-amplified MKN45 and SNU620 cells with concomitant induction of apoptosis, but not in c-MET-reduced MKN28 and AGS cells. Foretinib treatment also significantly reduced phosphor-c-MET, phosphor-AKT, beta-catenin, and COX-2 protein expression in MKN45 and SNU620 cells. Interestingly, foretinib significantly reduced CD44, CD44v9, COX-2, OCT3/4, CCND1, c-MYC, VEGFA, and HIF-1a gene expression in CD44 and MET coactivated MKN45 cells and increased CD44s gene expression; in contrast, these drugs were only slightly active against SNU620 cells.

conclusionThe results of this study indicate that foretinib could be a therapeutic agent for the prevention or treatment of GCs positive for CD44v9 and c-MET.

Indexed as

CD44v9c-METforetinibgastric cancerOCT3/4

Identifiers

PMID32099405
PMCPMC7006849
OpenAlexW3003840065

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.