Evidence map›Paper›PMID 24119769›Full record

ArticleJournal of translational medicine2013

Caveolin-1 in renal cell carcinoma promotes tumour cell invasion, and in co-operation with pERK predicts metastases in patients with clinically confined disease.

Lee Campbell, Ghaith Al-Jayyoussi, Robert Gutteridge, Nigel Gumbleton, Rosie Griffiths, Simon Gumbleton, Mathew W Smith, David F R Griffiths, Mark Gumbleton

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 22% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

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  7. Involvement of caveolin-1 in skin diseases.Frontiers in immunology · 2022
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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

9 authors at 1 institution in 1 country.

Lee CampbellCardiff School of Pharmacy and Pharmaceutical Sciences, Cardiff University, Cardiff CF10 3XF, UK. gumbleton@cf.ac.uk.
Ghaith Al-Jayyoussi
Robert Gutteridge
Nigel Gumbleton
Rosie Griffiths
Simon Gumbleton
Mathew W Smith
David F R Griffiths
Mark Gumbleton
Cardiff University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUp to 40% of patients initially diagnosed with clinically-confined renal cell carcinoma (RCC) and who undergo curative surgery will nevertheless relapse with metastatic disease (mRCC) associated with poor long term survival. The discovery of novel prognostic/predictive biomarkers and drug targets is needed and in this context the aim of the current study was to investigate a putative caveolin-1/ERK signalling axis in clinically confined RCC, and to examine in a panel of RCC cell lines the effects of caveolin-1 (Cav-1) on pathological processes (invasion and growth) and select signalling pathways.

methodsUsing immunohistochemistry we assessed the expression of both Cav-1 and phosphorylated-ERK (pERK) in 176 patients with clinically confined RCC, their correlation with histological parameters and their impact upon disease-free survival. Using a panel of RCC cell lines we explored the functional effects of Cav-1 knockdown upon cell growth, cell invasion and VEGF-A secretion, as well Cav-1 regulation by cognate cell signalling pathways.

resultsWe found a significant correlation (P = 0.03) between Cav-1 and pERK in a cohort of patients with clinically confined disease which represented a prognostic biomarker combination (HR = 4.2) that effectively stratified patients into low, intermediate and high risk groups with respect to relapse, even if the patients' tumours displayed low grade and/or low stage disease. In RCC cell lines Cav-1 knockdown unequivocally reduced cell invasive capacity while also displaying both pro-and anti-proliferative effects; targeted knockdown of Cav-1 also partially suppressed VEGF-A secretion in VHL-negative RCC cells. The actions of Cav-1 in the RCC cell lines appeared independent of both ERK and AKT/mTOR signalling pathways.

conclusionThe combined expression of Cav-1 and pERK serves as an independent biomarker signature with potential merit in RCC surveillance strategies able to predict those patients with clinically confined disease who will eventually relapse. In a panel of in-vitro RCC cells Cav-1 promotes cell invasion with variable effects on cell growth and VEGF-A secretion. Cav-1 has potential as a therapeutic target for the prevention and treatment of mRCC.

Indexed as

Carcinoma, Renal CellCaveolin 1Cell Line, TumorCell ProliferationDown-RegulationExtracellular Signal-Regulated MAP KinasesGene Knockdown TechniquesHumansKidney NeoplasmsMultivariate AnalysisNeoplasm InvasivenessNeoplasm MetastasisPhosphorylationPrognosisProportional Hazards ModelsProto-Oncogene Proteins c-aktCaveolin 1Extracellular Signal-Regulated MAP KinasesMTOR protein, humanProto-Oncogene Proteins c-aktRANK LigandTOR Serine-Threonine KinasesVascular Endothelial Growth Factor AVHL protein, humanVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID24119769
PMCPMC4015803
OpenAlexW2107196644

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.