Evidence map›Paper›PMID 19175685›Full record

ArticleJournal of cellular and molecular medicine2009

Invadopodia biogenesis is regulated by caveolin-mediated modulation of membrane cholesterol levels.

Giusi Caldieri, Giada Giacchetti, Galina Beznoussenko, Francesca Attanasio, Inmaculada Ayala, Roberto Buccione

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Review
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  7. Article
  8. Review
  9. Review
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  11. Article
  12. Different Role of Caveolin-1 Gene in the Progression of Gynecological Tumors.Asian Pacific journal of cancer prevention : APJCP · 2019
    Review
  13. Article
  14. Article
  15. Article
  16. Metastasis review: from bench to bedside.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Review
  17. Article
  18. Signaling inputs to invadopodia and podosomes.Journal of cell science · 2013
    Review
  19. Review
  20. Caveolin-1 as a promoter of tumour spreading: when, how, where and why.Journal of cellular and molecular medicine · 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

6 authors at 1 institution in 1 country.

Giusi CaldieriTumor Cell Invasion Laboratory, Department of Cell Biology and Oncology, Consorzio Mario Negri Sud, Chieti, Italy.
Giada GiacchettiTumor Cell Invasion Laboratory, Department of Cell Biology and Oncology, Consorzio Mario Negri Sud, Chieti, Italy.
Galina BeznoussenkoTumor Cell Invasion Laboratory, Department of Cell Biology and Oncology, Consorzio Mario Negri Sud, Chieti, Italy.
Francesca AttanasioTumor Cell Invasion Laboratory, Department of Cell Biology and Oncology, Consorzio Mario Negri Sud, Chieti, Italy.
Inmaculada AyalaTumor Cell Invasion Laboratory, Department of Cell Biology and Oncology, Consorzio Mario Negri Sud, Chieti, Italy.
Roberto BuccioneTumor Cell Invasion Laboratory, Department of Cell Biology and Oncology, Consorzio Mario Negri Sud, Chieti, Italy.
Mario Negri Sud Foundation · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Invadopodia are proteolytically active protrusions formed by invasive tumoural cells when grown on an extracellular matrix (ECM) substratum. Clearly, invadopodia are specialized membrane domains acting as sites of signal transduction and polarized delivery of components required for focalized ECM degradation. For these reasons, invadopodia are a model to study focal ECM degradation by tumour cells. We investigated the features of invadopodia membrane domains and how altering their composition would affect invadopodia biogenesis and function. This was achieved through multiple approaches including manipulation of the levels of cholesterol and other lipids at the plasma membrane, alteration of cholesterol trafficking by acting on caveolin 1 expression and phosphorylation. We show that cholesterol depletion impairs invadopodia formation and persistence, and that invadopodia themselves are cholesterol-rich membranes. Furthermore, the inhibition of invadopodia formation and ECM degradation after caveolin 1 knock-down was efficiently reverted by simple provision of cholesterol. In addition, the inhibitory effect of caveolin 3(DGV) expression, a mutant known to block cholesterol transport to the plasma membrane, was similarly reverted by provision of cholesterol. We suggest that invadopodia biogenesis, function and structural integrity rely on appropriate levels of plasma membrane cholesterol, and that invadopodia display the properties of cholesterol-rich membranes. Also, caveolin 1 exerts its function in invadopodia formation by regulating cholesterol balance at the plasma membrane. These findings support the connection between cholesterol, cancer and caveolin 1, provide further understanding of the role of cholesterol in cancer progression and suggest a mechanistic framework for the proposed anti-cancer activity of statins, tightly related to their blood cholesterol-lowering properties.

Indexed as

CaveolinsCell Line, TumorCholesterolHumansMelanomaMembrane LipidsNeoplasm InvasivenessNeoplasm MetastasisCaveolinsCholesterolMembrane Lipids

Identifiers

PMID19175685
PMCPMC6512369
OpenAlexW2093098592

What OpenQuestion 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 OpenQuestion graph.