Evidence map›Paper›PMID 17684486›Full record

ArticleOncogene2008

Silencing the MET oncogene leads to regression of experimental tumors and metastases.

S Corso, C Migliore, E Ghiso, G De Rosa, P M Comoglio, S Giordano

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 131 citations in OpenAlex.

  1. Review
  2. An Observatory for theCancers · 2023
    Review
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  15. Article
  16. Article
  17. Article
  18. MicroRNA and MET in lung cancer.Annals of translational medicine · 2015
    Review
  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

6 authors at 2 institutions in 1 country.

S CorsoDivision of Molecular Oncology, Institute for Cancer Research and Treatment (IRCC), University of Turin Medical School, Candiolo, Torino, Italy.
C Migliore
E Ghiso
G De Rosa
P M Comoglio
S Giordano
Candiolo Cancer Institute · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In spite of the established knowledge of the genetic alterations responsible for cancer onset, the genes promoting and maintaining the invasive/metastatic phenotype are still elusive. The MET proto-oncogene, encoding the tyrosine kinase receptor for hepatocyte growth factor (HGF), senses unfavorable micro-environmental conditions and drives cell invasion and metastasis. MET overexpression, often induced by tumor hypoxia, leads to constitutive activation of the receptor and correlates with poor prognosis. To establish the role of MET in different phases of tumor progression, we developed an inducible lentiviral delivery system of RNA interference. Silencing the endogenous MET gene, overexpressed in tumor cells, resulted in (i) impairment of the execution of the full invasive growth program in vitro, (ii) lack of tumor growth and (iii) decreased generation of experimental metastases in vivo. Notably, silencing MET in already established metastases led to their almost complete regression. This indicates that persistent expression of the MET oncogene is mandatory until the advanced phases of cancer progression.

Indexed as

Gene SilencingDisease ProgressionGene Expression Regulation, NeoplasticHumansLentivirusNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsProto-Oncogene MasProto-Oncogene Proteins c-metRNA InterferenceTumor Cells, CulturedMAS1 protein, humanProto-Oncogene MasProto-Oncogene Proteins c-met

Identifiers

PMID17684486
OpenAlexW2031981310

What OpenQuestion holds

Textmetadata
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.