Evidence map›Paper›PMID 22396494›Full record

ArticleCancer research2012

Genetic ablation of Cav1 differentially affects melanoma tumor growth and metastasis in mice: role of Cav1 in Shh heterotypic signaling and transendothelial migration.

Franco Capozza, Casey Trimmer, Remedios Castello-Cros, Sanjay Katiyar, Diana Whitaker-Menezes, Antonia Follenzi, Marco Crosariol, Gemma Llaverias, Federica Sotgia, Richard G Pestell and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Caveolae and signalling in cancer.Nature reviews. Cancer · 2015
    Review
  15. Review
  16. Article
  17. Caveolin-1 as a promoter of tumour spreading: when, how, where and why.Journal of cellular and molecular medicine · 2013
    Review
  18. Caveolae as plasma membrane sensors, protectors and organizers.Nature reviews. Molecular cell biology · 2013
    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

11 authors at 2 institutions in 2 countries.

Franco CapozzaDepartment of Cancer Biology, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Franco.Capozza@jefferson.edu
Casey Trimmer
Remedios Castello-Cros
Sanjay Katiyar
Diana Whitaker-Menezes
Antonia Follenzi
Marco Crosariol
Gemma Llaverias
Federica Sotgia
Richard G Pestell
Michael P Lisanti
Roma Tre University · ITThomas Jefferson University · US

Funding

CAV-1, Stat5a Signaling, and Estrogen-Dependent Breast CancerR01CA098779 · NCI · YESHIVA UNIVERSITY · PI FRANK, PHILIPPE G. · 2003 to 2012
$3.5M
TRAINING PROGRAMS IN MOLECULAR GENETICS OF CANCERT32CA009678 · NCI · THOMAS JEFFERSON UNIVERSITY · PI BUCHBERG, ARTHUR M. · 1992 to 2008
$2.3M
CAV-1 Epithelial-Stromal Interactions and Breast CancerR01CA120876 · NCI · THOMAS JEFFERSON UNIVERSITY · PI LISANTI, MICHAEL P · 2007 to 2011
$1.5M
NCI NIH HHS R01 CA098779NCI NIH HHS R01CA098779NCI NIH HHS R01 CA120876NCI NIH HHS R01CA120876NCI NIH HHS T32 CA009678NCI NIH HHS T32-CA09678
6 · The paper itself

Abstract

Both cell-autonomous and non-cell-autonomous factors contribute to tumor growth and metastasis of melanoma. The function of caveolin-1 (Cav1), a multifunctional scaffold protein known to modulate several biologic processes in both normal tissue and cancer, has been recently investigated in melanoma cancer cells, but its role in the melanoma microenvironment remains largely unexplored. Here, we show that orthotopic implantation of B16F10 melanoma cells in the skin of Cav1KO mice increases tumor growth, and co-injection of Cav1-deficient dermal fibroblasts with melanoma cells is sufficient to recapitulate the tumor phenotype observed in Cav1KO mice. Using indirect coculture experiments with fibroblasts and melanoma cells combined with cytokine analysis, we found that Cav1-deficient fibroblasts promoted the growth of melanoma cells via enhanced paracrine cytokine signaling. Specifically, Cav1-deficient fibroblasts displayed increased ShhN expression, which heterotypically enhanced the Shh signaling pathway in melanoma cells. In contrast to primary tumor growth, the ability of B16F10 melanoma cells to form lung metastases was significantly reduced in Cav1KO mice. This phenotype was associated mechanistically with the inability of melanoma cells to adhere to and to transmigrate through a monolayer of endothelial cells lacking Cav1. Together, our findings show that Cav1 may regulate different mechanisms during primary melanoma tumor growth and metastatic dissemination.

Indexed as

AnimalsCaveolin 1Caveolin 2Cell Growth ProcessesCell MovementCoculture TechniquesCytokinesFemaleFibroblastsHedgehog ProteinsHumansHuman Umbilical Vein Endothelial CellsLung NeoplasmsMelanoma, ExperimentalMiceMice, Inbred C57BLCav1 protein, mouseCav2 protein, mouseCaveolin 1Caveolin 2CytokinesHedgehog ProteinsShh protein, mouse

Identifiers

PMID22396494
PMCPMC3342428
OpenAlexW2109293062

What OpenQuestion holds

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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.