Evidence map›Paper›PMID 12856716›Full record

ArticleClinical & experimental metastasis2003

Activation of c-Met in colorectal carcinoma cells leads to constitutive association of tyrosine-phosphorylated beta-catenin.

Matthew H Herynk, Rachael Tsan, Robert Radinsky, Gary E Gallick

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical & experimental metastasis, 2003. 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
–field-weighted citation impact
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.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Meeting the biologic challenge of colorectal metastases.Clinical & experimental metastasis · 2012
    Review
  7. Article
  8. Decorin: a guardian from the matrix.The American journal of pathology · 2012
    Review
  9. Proteoglycans in cancer biology, tumour microenvironment and angiogenesis.Journal of cellular and molecular medicine · 2011
    Review
  10. Article
  11. Article
  12. Targeting the Met signaling pathway in renal cancer.Expert review of anticancer therapy · 2009
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. The von Hippel-Lindau tumor suppressor gene product represses oncogenic beta-catenin signaling in renal carcinoma cells.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  18. Article
  19. Article
  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

4 authors.

Matthew H HerynkDepartment of Cancer Biology, University of Texas M. D. Anderson Cancer Center, Houston 77401, USA.
Rachael Tsan
Robert Radinsky
Gary E Gallick

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
SRC KINASES IN COLON TUMORIGENESIS AND METASTASISR01CA065527 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI GALLICK, GARY E · 1996 to 2003
$881k
TRAINING IN INTERDISCIPLINARY STUDIES IN CANCER BIOLOGYT32CA060440 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI GRIMM, ELIZABETH A · 1993 to 2002
$424k
MOLECULAR REGUL OF HUMAN COLON CANCER LIVER METASTASISR29CA067952 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI RADINSKY, ROBERT · 1995 to 1999
–
NCI NIH HHS CA16672NCI NIH HHS CA65527NCI NIH HHS CA67952NCI NIH HHS T32CA60440-9
6 · The paper itself

Abstract

Increased expression and/or activity of c-Met, the receptor protein tyrosine kinase for hepatocyte growth factor/scatter factor, occurs commonly during colon tumor progression. To examine potential roles for c-Met in promoting metastasis, we compared the colon tumor cell line KM12C with low metastatic potential to the isogenic variants KM,12L4 and KM12SM with high metastatic potential. KM12C cells express c-Met with low levels of tyrosine phosphorylation in the absence of HGF. The high metastatic cells express a c-Met that is constitutively tyrosine phosphorylated, they have increased colony formation, and are minimally responsive to HGF relative to the parental cells. Tyrosine-phosphorylated beta-catenin was constitutively associated with c-Met in the more metastatic cells, but was inducible only after HGF addition in the less metastatic cells. Functions mediated by beta-catenin, including cell-cell adhesion and migration, and activation of the tcf (T-cell factor) family of transcription factors, were also elevated in the more metastatic KM12SM and L4 cells. Furthermore, analysis of the known tcf transcriptional target genes, cyclin D1, c-Myc, and uPAR, demonstrated increased expression in the high metastatic cells, correlating with the levels of tcf activity. Collectively, these results suggest that endogenous activation of c-Met in highly metastatic KM12SM CRC cells results in increased survival and growth under anchorage independent conditions, increased in vitro migration, and elevated levels of tcf target genes. Thus, beta-catenin association with activated c-Met may contribute to a more aggressive liver metastatic phenotype of these cells.

Indexed as

beta CateninBlotting, WesternCell AdhesionCell MovementColony-Forming Units AssayColorectal NeoplasmsCyclin D1Cytoskeletal ProteinsGene Expression Regulation, NeoplasticHepatocyte Growth FactorHumansLuciferasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesMutationbeta CateninCTNNB1 protein, humanCyclin D1Cytoskeletal ProteinsHepatocyte Growth FactorLuciferasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-metTrans-ActivatorsTyrosine

Identifiers

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Registered trials

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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.