Evidence map›Paper›PMID 24823486›Full record

ArticlePloS one2014

Activation of c-Met and upregulation of CD44 expression are associated with the metastatic phenotype in the colorectal cancer liver metastasis model.

Victoria A Elliott, Piotr Rychahou, Yekaterina Y Zaytseva, B Mark Evers

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.9field-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, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Liver Tropism in Cancer: The Hepatic Metastatic Niche.Cold Spring Harbor perspectives in medicine · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Upregulation of c-mesenchymal epithelial transition expression andExperimental and therapeutic medicine · 2018
    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 at 2 institutions in 1 country.

Victoria A ElliottMarkey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America.
Piotr RychahouMarkey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America; Department of Surgery, University of Kentucky, Lexington, Kentucky, United States of America.
Yekaterina Y ZaytsevaMarkey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America.
B Mark EversMarkey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America; Department of Surgery, University of Kentucky, Lexington, Kentucky, United States of America.
Markey Cancer Center · USUniversity of Kentucky · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
SURGICAL STUDIES OF FUNCTIONAL GENE EXPRESSIONR01DK048498 · NIDDK · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI EVERS, BERNARD MARK · 1996 to 2023
$7.9M
Interdisciplinary Research Training in Cancer BiologyT32CA165990 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers, KATHLEEN L. O'CONNOR · 2013 to 2026
$3.2M
NCI NIH HHS P30 CA177558NCI NIH HHS T32 CA165990NCI NIH HHS T32CA165990NIDDK NIH HHS R01 DK048498NIDDK NIH HHS R01DK048498
6 · The paper itself

Abstract

backgroundLiver metastasis is the most common cause of death in patients with colorectal cancer. Despite extensive research into the biology of cancer progression, the molecular mechanisms that drive colorectal cancer metastasis are not well characterized.

methodsHT29 LM1, HT29 LM2, HT29 LM3 cell lines were derived from the human colorectal cancer cell line HT29 following multiple rounds of in vivo selection in immunodeficient mice.

resultsCD44 expression, a transmembrane glycoprotein involved in cell-cell and cell-matrix adhesions, and cancer cells adhesion to endothelial cells was increased in all in vivo selected cell lines, with maximum CD44 expression and cancer cells adhesion to endothelial cells in the highly metastatic HT29 LM3 cell line. Activation of c-Met upon hepatocyte growth factor (HGF) stimulation in the in vivo selected cell lines is CD44 independent. In vitro separation of CD44 high and low expression cells from HT29 LM3 cell line with FACS sorting confirmed that c-Met activation is CD44 independent upon hepatocyte growth factor stimulation. Furthermore, in vivo evaluation of CD44 low and high expressing HT29 LM3 cells demonstrated no difference in liver metastasis penetrance.

conclusionsTaken together, our findings indicate that the aggressive metastatic phenotype of in vivo selected cell lines is associated with overexpression of CD44 and activation of c-MET. We demonstrate that c-Met activation is CD44 independent upon hepatocyte growth factor stimulation and confirm that CD44 expression in HT29 LM3 cell line is not responsible for the increase in metastatic penetrance in HT29 LM3 cell line.

Indexed as

AnimalsBlotting, WesternCell AdhesionCell Line, TumorColorectal NeoplasmsFlow CytometryGene Expression Regulation, NeoplasticHepatocyte Growth FactorHumansHyaluronan ReceptorsImmunohistochemistryLiver NeoplasmsMiceProto-Oncogene Proteins c-metCD44 protein, humanHepatocyte Growth FactorHyaluronan ReceptorsProto-Oncogene Proteins c-met

Identifiers

PMID24823486
PMCPMC4019574
OpenAlexW1997766443

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.