Evidence map›Paper›PMID 29210059›Full record

ArticleInternational journal of cancer2018

Ezrin mediates both HGF/Met autocrine and non-autocrine signaling-induced metastasis in melanoma.

Liping Huang, Yifei Qin, Qiang Zuo, Kavita Bhatnagar, Jingbo Xiong, Glenn Merlino, Yanlin Yu

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  7. Review
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  10. Review
  11. Pathophysiological Roles of Actin-Binding Scaffold Protein, Ezrin.International journal of molecular sciences · 2022
    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

7 authors at 2 institutions in 2 countries.

Liping HuangLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institutes, National Institutes of Health, Bethesda, MD, 20892-4264.
Yifei QinLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institutes, National Institutes of Health, Bethesda, MD, 20892-4264.
Qiang ZuoLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institutes, National Institutes of Health, Bethesda, MD, 20892-4264.
Kavita BhatnagarLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institutes, National Institutes of Health, Bethesda, MD, 20892-4264.
Jingbo XiongDepartment of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, People's Republic of China.
Glenn MerlinoLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institutes, National Institutes of Health, Bethesda, MD, 20892-4264.
Yanlin YuLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institutes, National Institutes of Health, Bethesda, MD, 20892-4264.ORCID 0000-0003-1513-3343
National Institutes of Health · USSouthern Medical University · CN

Funding

Genetically Engineered Mouse Models to Study RTK Function in MelanomaZIABC008756 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MERLINO, GLENN T. · 2009 to 2024
$17.7M
Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

Aberrant HGF/Met signaling promotes tumor migration, invasion, and metastasis through both autocrine and non-autocrine mechanisms; however, the molecular downstream signaling mechanisms by which HGF/Met induces metastasis are incompletely understood. We here report that Ezrin expression is stimulated by HGF and correlates with activated HGF/Met, indicating that HGF/Met signaling regulates the expression of Ezrin. We show that HGF/Met signaling activates the transcription factor Sp1 through the MAPK pathway, and activated Sp1 can in turn directly bind to the promoter of Ezrin gene and regulate its transcription. Notably, knockdown of Ezrin expression by shRNAs inhibits the metastasis induced by either HGF/Met autocrine or non-autocrine signaling in syngeneic wildtype and HGF transgenic mouse hosts. We also used small molecule drugs in preclinical mouse models to confirm that Ezrin is one of the downstream molecules mediating HGF/Met signaling-induced metastasis in melanoma. We conclude that Ezrin is a key downstream factor involved in the regulation of HGF/Met signaling-induced metastasis and demonstrate a link between Ezrin and HGF/Met/MAPK/Sp1 activation in the metastatic process. Our data indicate that Ezrin represents a promising therapeutic target for patients bearing tumors with activated HGF/Met signaling.

Indexed as

AnimalsAutocrine CommunicationCell Line, TumorCell MovementCytoskeletal ProteinsEzrinHepatocyte Growth FactorMaleMelanomaMiceMice, Inbred C57BLNeoplasm MetastasisPromoter Regions, GeneticProto-Oncogene Proteins c-metSignal TransductionCytoskeletal ProteinsEzrinHepatocyte Growth FactorProto-Oncogene Proteins c-metEzrinHGFmelanomametastasistherapeutic target

Identifiers

PMID29210059
PMCPMC5814345
OpenAlexW2774550979

What OpenQuestion holds

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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.