Evidence map›Paper›PMID 23267770›Full record

ArticleThe American journal of pathology2013

Cav1 suppresses tumor growth and metastasis in a murine model of cutaneous SCC through modulation of MAPK/AP-1 activation.

Casey Trimmer, Gloria Bonuccelli, Sanjay Katiyar, Federica Sotgia, Richard G Pestell, Michael P Lisanti, Franco Capozza

Abstract read
In one paragraph

Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Involvement of caveolin-1 in skin diseases.Frontiers in immunology · 2022
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Rho/ROCK Pathway Regulates Migration and Invasion of Esophageal Squamous Cell Carcinoma by Regulating Caveolin-1.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  10. Article
  11. Article
  12. Review
  13. Genetic variations of CAV1 gene contribute to HCC risk: a case-control study.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  14. 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

7 authors.

Casey TrimmerDepartment of Cancer Biology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Gloria Bonuccelli
Sanjay Katiyar
Federica Sotgia
Richard G Pestell
Michael P Lisanti
Franco Capozza

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 R01-CA-098779NCI NIH HHS R01 CA120876NCI NIH HHS R01CA120876NCI NIH HHS T32 CA009678NCI NIH HHS T32-CA09678
6 · The paper itself

Abstract

Caveolin-1 (Cav1) is a scaffolding protein that serves to regulate the activity of several signaling molecules. Its loss has been implicated in the pathogenesis of several types of cancer, but its role in the development and progression of cutaneous squamous cell carcinoma (cSCC) remains largely unexplored. Herein, we use the keratinocyte cell line PAM212, a murine model of cSCC, to determine the function of Cav1 in skin tumor biology. We first show that Cav1 overexpression decreases cell and tumor growth, whereas Cav1 knockdown increases these attributes in PAM212 cells. In addition, Cav1 knockdown increases the invasive ability and incidence of spontaneous lymph node metastasis. Finally, we demonstrate that Cav1 knockdown increases extracellular signaling-related kinase 1/2 mitogen-activated protein kinase/activator protein-1 pathway activation. We attribute the growth and invasive advantage conferred by Cav1 knockdown to increased expression of activator protein-1 transcriptional targets, including cyclin D1 and keratin 18, which show inverse expression in PAM212 based on the expression level of Cav1. In summary, we demonstrate that loss of Cav1 affects several characteristics associated with aggressive human skin tumors and that this protein may be an important modulator of tumor growth and invasion in cSCC.

Indexed as

AnimalsCarcinoma, Squamous CellCaveolin 1Cell Line, TumorCell MovementCell ProliferationDisease Models, AnimalEnzyme ActivationEpidermal Growth FactorGene Knockdown TechniquesHumansKeratin-18KeratinocytesMAP Kinase Signaling SystemMiceMice, Inbred BALB CCaveolin 1Epidermal Growth FactorKeratin-18Mitogen-Activated Protein KinasesTranscription Factor AP-1

Identifiers

PMID23267770
PMCPMC3586688

What Socratic 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 Socratic graph.