Evidence map›Paper›PMID 27779808›Full record

ArticleCancer science2016

Functional and therapeutic relevance of hepatocyte growth factor/c-MET signaling in synovial sarcoma.

Yoshinori Imura, Takaaki Nakai, Shutaro Yamada, Hidetatsu Outani, Satoshi Takenaka, Kenichiro Hamada, Nobuhito Araki, Kazuyuki Itoh, Hideki Yoshikawa, Norifumi Naka

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-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

22 citing papers in PubMed, 31 citations in OpenAlex.

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  4. Angiogenic signaling pathways and anti-angiogenic therapy for cancer.Signal transduction and targeted therapy · 2023
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  11. Review
  12. MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers.Frontiers in cell and developmental biology · 2020
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Increased Expression of c-Met is Associated with Chemotherapy-Resistant Breast Cancer and Poor Clinical Outcome.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  18. Article
  19. Review
  20. 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

10 authors at 2 institutions in 1 country.

Yoshinori ImuraDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Takaaki NakaiDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Shutaro YamadaDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Hidetatsu OutaniMusculoskeletal Oncology Service, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka, Japan.
Satoshi TakenakaDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Kenichiro HamadaDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Nobuhito ArakiMusculoskeletal Oncology Service, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka, Japan.
Kazuyuki ItohBiology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka, Japan.
Hideki YoshikawaDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Norifumi NakaDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Osaka University · JPOsaka Medical Center for Cancer and Cardiovascular Diseases · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synovial sarcoma (SS) is an aggressive soft tissue sarcoma with a poor prognosis and, thus, novel therapeutic strategies for SS are urgently required. In the present study, we investigated the functional and therapeutic relevance of hepatocyte growth factor (HGF)/c-MET signaling in SS. Both HGF and c-MET were highly expressed in Yamato-SS cells, resulting in activation of c-MET and its downstream AKT and extracellular signal-regulated kinase signaling pathways, whereas c-MET was expressed but not activated in SYO-1 or HS-SY-II cells. c-MET-activated Yamato-SS cells showed higher anchorage-independent growth ability and less sensitivity to chemotherapeutic agents than did c-MET-inactivated SYO-1 or HS-SY-II cells. INC280, a selective c-MET inhibitor, inhibited growth of Yamato-SS cells both in vitro and in vivo but not that of SYO-1 or HS-SY-II cells. INC280 induced cell cycle arrest and apoptosis, and blocked phosphorylation of c-MET and its downstream effectors in Yamato-SS cells. Co-expression of HGF and c-MET in SS clinical samples correlated with a poor prognosis in patients with SS. Taken together, activation of HGF/c-MET signaling in an autocrine fashion leads to an aggressive phenotype in SS and targeting of this signaling exerts superior antitumor effects on c-MET-activated SS. HGF/c-MET expression status is a potential biomarker for identification of SS patients with a worse prognosis who can benefit from c-MET inhibitors.

Indexed as

Signal TransductionAnimalsAntineoplastic AgentsAutocrine CommunicationCell Line, TumorCell ProliferationDisease Models, AnimalGene ExpressionGene SilencingHepatocyte Growth FactorHeterograftsHumansMicePrognosisProtein Kinase InhibitorsProto-Oncogene Proteins c-metAntineoplastic AgentsHepatocyte Growth FactorProtein Kinase InhibitorsProto-Oncogene Proteins c-metc-METhepatocyte growth factorINC280synovial sarcomaYamato-SS

Identifiers

PMID27779808
PMCPMC5198956
OpenAlexW2539434301

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.