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Follistatin is a metastasis suppressor in a mouse model of HER2-positive breast cancer

Overview of attention for article published in Breast Cancer Research, June 2017
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1 tweeter

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Title
Follistatin is a metastasis suppressor in a mouse model of HER2-positive breast cancer
Published in
Breast Cancer Research, June 2017
DOI 10.1186/s13058-017-0857-y
Pubmed ID
Authors

Darcie D. Seachrist, Steven T. Sizemore, Emhonta Johnson, Fadi W. Abdul-Karim, Kristen L. Weber Bonk, Ruth A. Keri

Abstract

Follistatin (FST) is an intrinsic inhibitor of activin, a member of the transforming growth factor-β superfamily of ligands. The prognostic value of FST and its family members, the follistatin-like (FSTL) proteins, have been studied in various cancers. However, these studies, as well as limited functional analyses of the FSTL proteins, have yielded conflicting results on the role of these proteins in disease progression. Furthermore, very few have been focused on FST itself. We assessed whether FST may be a suppressor of tumorigenesis and/or metastatic progression in breast cancer. Using publicly available gene expression data, we examined the expression patterns of FST and INHBA, a subunit of activin, in normal and cancerous breast tissue and the prognostic value of FST in breast cancer metastases, recurrence-free survival, and overall survival. The functional effects of activin and FST on in vitro proliferation, migration, and invasion of breast cancer cells were also examined. FST overexpression in an autochthonous mouse model of breast cancer was then used to assess the in vivo impact of FST on metastatic progression. Examination of multiple breast cancer datasets revealed that FST expression is reduced in breast cancers compared with normal tissue and that low FST expression predicts increased metastasis and reduced overall survival. FST expression was also reduced in a mouse model of HER2/Neu-induced metastatic breast cancer. We found that FST blocks activin-induced breast epithelial cell migration in vitro, suggesting that its loss may promote breast cancer aggressiveness. To directly determine if FST restoration could inhibit metastatic progression, we transgenically expressed FST in the HER2/Neu model. Although FST had no impact on tumor initiation or growth, it completely blocked the formation of lung metastases. These data indicate that FST is a bona fide metastasis suppressor in this mouse model and support future efforts to develop an FST mimetic to suppress metastatic progression.

Twitter Demographics

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

Mendeley readers

The data shown below were compiled from readership statistics for 18 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 18 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 4 22%
Researcher 3 17%
Student > Master 3 17%
Student > Doctoral Student 2 11%
Student > Bachelor 1 6%
Other 5 28%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 28%
Agricultural and Biological Sciences 4 22%
Veterinary Science and Veterinary Medicine 2 11%
Pharmacology, Toxicology and Pharmaceutical Science 2 11%
Unspecified 1 6%
Other 2 11%
Unknown 2 11%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. 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 06 June 2017.
All research outputs
#7,043,514
of 11,317,953 outputs
Outputs from Breast Cancer Research
#910
of 1,293 outputs
Outputs of similar age
#150,716
of 267,496 outputs
Outputs of similar age from Breast Cancer Research
#17
of 21 outputs
Altmetric has tracked 11,317,953 research outputs across all sources so far. This one is in the 23rd percentile – i.e., 23% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,293 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 9.9. This one is in the 22nd percentile – i.e., 22% 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 267,496 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 34th percentile – i.e., 34% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 21 others from the same source and published within six weeks on either side of this one. This one is in the 19th percentile – i.e., 19% of its contemporaries scored the same or lower than it.