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Involvement of gelsolin in TGF-beta 1 induced epithelial to mesenchymal transition in breast cancer cells

Overview of attention for article published in Journal of Biomedical Science, October 2015
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Title
Involvement of gelsolin in TGF-beta 1 induced epithelial to mesenchymal transition in breast cancer cells
Published in
Journal of Biomedical Science, October 2015
DOI 10.1186/s12929-015-0197-0
Pubmed ID
Authors

Zhi-Yuan Chen, Pei-Wen Wang, Dar-Bin Shieh, Kuan-Ying Chiu, Ying-Ming Liou

Abstract

Increasing evidence suggests that transforming growth factor-beta 1 (TGF-β1) triggers epithelial to mesenchymal transition (EMT) and facilitates breast cancer stem cell differentiation. Gelsolin (GSN) is a ubiquitous actin filament-severing protein. However, the relationship between the expression level of GSN and the TGF-β signaling for EMT progression in breast cancer cells is not clear. TGF-β1 acted on MDA-MB231 breast cancer cells by decreasing cell proliferation, changing cell morphology to a fibroblast-like shape, increasing expressions for CD44 and GSN, and increasing EMT expression and cell migration/invasion. Study with GSN overexpression (GSN op) in both MDA-MB231 and MCF-7 cells demonstrated that increased GSN expression resulted in alterations of cell proliferation and cell cycle progression, modification of the actin filament assembly associated with altering cell surface elasticity and cell detachment in these breast cancer cells. In addition, increased cell migration was found in GSN op MDA-MB231 cells. Studies with GSN op and silencing by small interfering RNA verified that GSN could modulate the expression of vimentin. Sorted by flow cytometry, TGF-β1 increased subpopulation of CD44+/CD22- cells increasing their expressions for GSN, Nanog, Sox2, Oct4, N-cadherin, and vimentin but decreasing the E-cadherin expression. Methylation specific PCR analysis revealed that TGF-β1 decreased 50 % methylation but increased 3-fold unmethylation on the GSN promoter in CD44+/CD22- cells. Two DNA methyltransferases, DNMT1and DNMT3B were also inhibited by TGF-β1. TGF-β1 induced epigenetic modification of GSN could alter the EMT process in breast cancer cells.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 53 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Estonia 1 2%
Unknown 52 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 13 25%
Student > Master 13 25%
Researcher 7 13%
Professor 2 4%
Student > Postgraduate 2 4%
Other 6 11%
Unknown 10 19%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 14 26%
Medicine and Dentistry 10 19%
Agricultural and Biological Sciences 6 11%
Pharmacology, Toxicology and Pharmaceutical Science 4 8%
Environmental Science 1 2%
Other 7 13%
Unknown 11 21%
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 October 2015.
All research outputs
#16,720,137
of 25,371,288 outputs
Outputs from Journal of Biomedical Science
#709
of 1,100 outputs
Outputs of similar age
#166,996
of 294,420 outputs
Outputs of similar age from Journal of Biomedical Science
#14
of 25 outputs
Altmetric has tracked 25,371,288 research outputs across all sources so far. This one is in the 32nd percentile – i.e., 32% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,100 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 11.0. This one is in the 31st percentile – i.e., 31% 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 294,420 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 25 others from the same source and published within six weeks on either side of this one. This one is in the 32nd percentile – i.e., 32% of its contemporaries scored the same or lower than it.