Evidence map›Paper›PMID 27683122›Full record

ArticleOncotarget2016

Different growth and metastatic phenotypes associated with a cell-intrinsic change of Met in metastatic melanoma.

Eri Adachi, Katsuya Sakai, Takumi Nishiuchi, Ryu Imamura, Hiroki Sato, Kunio Matsumoto

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Exosome application in tumorigenesis: diagnosis and treatment of melanoma.Medical oncology (Northwood, London, England) · 2022
    Review
  5. Article
  6. Role of extracellular vesicles in tumour microenvironment.Cell communication and signaling : CCS · 2020
    Review
  7. Review
  8. Article
  9. HGF/c-MET Signaling in Melanocytes and Melanoma.International journal of molecular sciences · 2018
    Review
  10. Review
  11. Role for extracellular vesicles in the tumour microenvironment.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018
    Review
  12. The key role of extracellular vesicles in the metastatic process.Biochimica et biophysica acta. Reviews on cancer · 2018
    Review
  13. Article
  14. Review
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 1 institution in 1 country.

Eri AdachiDivision of Tumor Dynamics and Regulation, Cancer Research Institute, Kanazawa University, Kakuma, Kanazawa 920-1192, Japan.
Katsuya SakaiDivision of Tumor Dynamics and Regulation, Cancer Research Institute, Kanazawa University, Kakuma, Kanazawa 920-1192, Japan.
Takumi NishiuchiDivision of Functional Genomics, Advanced Science Research Center, Kanazawa University, Kakuma, Kanazawa 920-0934, Japan.
Ryu ImamuraDivision of Tumor Dynamics and Regulation, Cancer Research Institute, Kanazawa University, Kakuma, Kanazawa 920-1192, Japan.
Hiroki SatoDivision of Tumor Dynamics and Regulation, Cancer Research Institute, Kanazawa University, Kakuma, Kanazawa 920-1192, Japan.
Kunio MatsumotoDivision of Tumor Dynamics and Regulation, Cancer Research Institute, Kanazawa University, Kakuma, Kanazawa 920-1192, Japan.
Kanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A dynamic phenotypic change contributes to the metastatic progression and drug resistance in malignant melanoma. Nevertheless, mechanisms for a phenotypic change have remained to be addressed. Here, we show that Met receptor expression changes in a cell-autonomous manner and can distinguish phenotypical differences in growth, as well as in metastatic and drug-resistant characteristics. In metastatic melanoma, the cells are composed of Met-low and Met-high populations. Met-low populations have stem-like gene expression profiles, are resistant to chemotherapeutic agents, and have shown abundant angiogenesis and rapid tumor growth in subcutaneous inoculation. Met-high populations have a differentiated phenotype, are relatively resistant to B-RAF inhibitor, and are highly metastatic to the lungs. Met plays a definitive role in lung metastasis because the lung metastasis of Met-high cells requires Met, and treatment of mice with the Met-containing exosomes from Met-high cells facilitates lung metastasis by Met-low cells. Clonal cell fate analysis showed the hierarchical phenotypical changes from Met-low to Met-high populations. Met-low cells either showed self-renewal or changed into Met-high cells, whereas Met-high cells remained Met-high. Clonal transition from Met-low to Met-high cells accompanied changes in the gene expression profile, in tumor growth, and in metastasis that were similar to those in Met-high cells. These findings indicate that malignant melanoma has the ability to undergo phenotypic change by a cell-intrinsic/autonomous mechanism that can be characterized by Met expression.

Indexed as

AnimalsAntineoplastic AgentsCarcinogenesisCell Line, TumorCell SeparationCell SurvivalDrug Resistance, NeoplasmExosomesFemaleFlow CytometryGene Expression ProfilingHumansIndolesLungLung NeoplasmsMelanomaAntineoplastic AgentsBRAF protein, humanIndolesMET protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-metRNA, Small InterferingSulfonamidesVemurafenibdrug resistanceHGFmalignant melanomametmetastasis

Identifiers

PMID27683122
PMCPMC5342589
OpenAlexW2523675486

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.