↓ Skip to main content

Phosphocaveolin-1 Enforces Tumor Growth and Chemoresistance in Rhabdomyosarcoma

Overview of attention for article published in PLOS ONE, January 2014
Altmetric Badge

About this Attention Score

  • Average Attention Score compared to outputs of the same age
  • Average Attention Score compared to outputs of the same age and source

Mentioned by

twitter
1 X user
peer_reviews
1 peer review site

Citations

dimensions_citation
18 Dimensions

Readers on

mendeley
33 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
Phosphocaveolin-1 Enforces Tumor Growth and Chemoresistance in Rhabdomyosarcoma
Published in
PLOS ONE, January 2014
DOI 10.1371/journal.pone.0084618
Pubmed ID
Authors

Fiorella Faggi, Stefania Mitola, Guglielmo Sorci, Francesca Riuzzi, Rosario Donato, Silvia Codenotti, Pietro Luigi Poliani, Manuela Cominelli, Raffaella Vescovi, Stefania Rossi, Stefano Calza, Marina Colombi, Fabio Penna, Paola Costelli, Ilaria Perini, Maurilio Sampaolesi, Eugenio Monti, Alessandro Fanzani

Abstract

Caveolin-1 (Cav-1) can ambiguously behave as either tumor suppressor or oncogene depending on its phosphorylation state and the type of cancer. In this study we show that Cav-1 was phosphorylated on tyrosine 14 (pCav-1) by Src-kinase family members in various human cell lines and primary mouse cultures of rhabdomyosarcoma (RMS), the most frequent soft-tissue sarcoma affecting childhood. Cav-1 overexpression in the human embryonal RD or alveolar RH30 cells yielded increased pCav-1 levels and reinforced the phosphorylation state of either ERK or AKT kinase, respectively, in turn enhancing in vitro cell proliferation, migration, invasiveness and chemoresistance. In contrast, reducing the pCav-1 levels by administration of a Src-kinase inhibitor or through targeted Cav-1 silencing counteracted the malignant in vitro phenotype of RMS cells. Consistent with these results, xenotransplantation of Cav-1 overexpressing RD cells into nude mice resulted in substantial tumor growth in comparison to control cells. Taken together, these data point to pCav-1 as an important and therapeutically valuable target for overcoming the progression and multidrug resistance of RMS.

X Demographics

X Demographics

The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 33 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Spain 1 3%
Portugal 1 3%
Unknown 31 94%

Demographic breakdown

Readers by professional status Count As %
Professor > Associate Professor 7 21%
Researcher 5 15%
Student > Ph. D. Student 5 15%
Student > Master 4 12%
Student > Bachelor 3 9%
Other 3 9%
Unknown 6 18%
Readers by discipline Count As %
Agricultural and Biological Sciences 8 24%
Biochemistry, Genetics and Molecular Biology 7 21%
Medicine and Dentistry 4 12%
Psychology 2 6%
Mathematics 1 3%
Other 0 0%
Unknown 11 33%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 26 August 2014.
All research outputs
#14,187,012
of 22,739,983 outputs
Outputs from PLOS ONE
#116,053
of 194,087 outputs
Outputs of similar age
#173,136
of 304,956 outputs
Outputs of similar age from PLOS ONE
#2,973
of 5,368 outputs
Altmetric has tracked 22,739,983 research outputs across all sources so far. This one is in the 35th percentile – i.e., 35% of other outputs scored the same or lower than it.
So far Altmetric has tracked 194,087 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 15.1. This one is in the 36th percentile – i.e., 36% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 304,956 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 40th percentile – i.e., 40% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 5,368 others from the same source and published within six weeks on either side of this one. This one is in the 41st percentile – i.e., 41% of its contemporaries scored the same or lower than it.