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Attention Score in Context
| Title |
Acquisition of epithelial-mesenchymal transition phenotype in the tamoxifen-resistant breast cancer cell: a new role for G protein-coupled estrogen receptor in mediating tamoxifen resistance through cancer-associated fibroblast-derived fibronectin and β1-integrin signaling pathway in tumor cells
|
|---|---|
| Published in |
Breast Cancer Research, May 2015
|
| DOI | 10.1186/s13058-015-0579-y |
| Pubmed ID | |
| Authors |
Jie Yuan, Manran Liu, Li Yang, Gang Tu, Qing Zhu, Maoshan Chen, Hong Cheng, Haojun Luo, Weijie Fu, Zhenhua Li, Guanglun Yang |
| Abstract |
Acquired tamoxifen resistance remains the major obstacle to breast cancer endocrine therapy. β1-integrin was identified as one of the target genes of G protein-coupled estrogen receptor (GPER), a novel estrogen receptor recognized as an initiator of tamoxifen resistance. Here, we investigated the role of β1-integrin in GPER-mediated tamoxifen resistance in breast cancer. The expression of β1-integrin and biomarkers of epithelial-mesenchymal transition (EMT) were evaluated immunohistochemically in 53 specimens of metastases (MTs) and paired primary tumors (PTs). The function of β1-integrin was investigated in tamoxifen-resistant (MCF-7R) subclones, derived from parental MCF-7 cells, and MCF-7R β1-integrin-silenced subclones in MTT and Transwell assays. Involved signaling pathways were identified using specific inhibitors and Western blotting analysis. GPER, β1-integrin and mesenchymal biomarkers (vimentin and fibronectin) expression in MTs increased compared to the corresponding PTs; a close expression pattern of β1-integrin and GPER were in MTs. Increased β1-integrin expression was also confirmed in MCF-7R cells compared with MCF-7 cells. This upregulation of β1-integrin was induced by agonists of GPER and blocked by both antagonist and knockdown of it in MCF-7R cells. Moreover, epidermal growth factor receptor/extracellular regulated protein kinase (EGFR/ERK) signaling pathway was involved in this transcriptional regulation since specific inhibitors of these kinases also reduced the GPER-induced upregulaiton of β1-integrin. Interestingly, silencing of β1-integrin partially rescued the sensitivity of MCF-7R cells to tamoxifen and α5β1-integrin subunit is probably responsible for this phenomenon. Importantly, the cell migration and EMT induced by cancer-associated fibroblasts (CAFs), or the product of CAFs, fibronectin, were reduced by knockdown of β1-integrin in MCF-7R cells. In addition, the downstream kinases of β1-integrin including focal adhesion kinase (FAK), Src and AKT were activated in MCF-7R cells and maybe involved in the interaction between cancer cells and CAFs. GPER/EGFR/ERK signaling upregulates β1-integrin expression and activates downstream kinases, which contributes to CAF-induced cell migration and EMT, in MCF-7R cells. GPER probably contributes to tamoxifen resistance via interaction with the tumor microenvironment in a β1-integrin dependent pattern. Thus, β1-integrin may be a potential target to improve anti-hormone therapy responses in breast cancer patients. |
Mendeley readers
The data shown below were compiled from readership statistics for 82 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Mexico | 1 | 1% |
| United States | 1 | 1% |
| Poland | 1 | 1% |
| Unknown | 79 | 96% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 17 | 21% |
| Researcher | 13 | 16% |
| Student > Master | 11 | 13% |
| Student > Doctoral Student | 8 | 10% |
| Student > Postgraduate | 6 | 7% |
| Other | 13 | 16% |
| Unknown | 14 | 17% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 25 | 30% |
| Agricultural and Biological Sciences | 18 | 22% |
| Medicine and Dentistry | 11 | 13% |
| Immunology and Microbiology | 2 | 2% |
| Pharmacology, Toxicology and Pharmaceutical Science | 2 | 2% |
| Other | 7 | 9% |
| Unknown | 17 | 21% |
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 24 August 2017.
All research outputs
#17,289,387
of 25,377,790 outputs
Outputs from Breast Cancer Research
#1,536
of 2,054 outputs
Outputs of similar age
#168,199
of 280,401 outputs
Outputs of similar age from Breast Cancer Research
#28
of 38 outputs
Altmetric has tracked 25,377,790 research outputs across all sources so far. This one is in the 21st percentile – i.e., 21% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,054 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 12.2. This one is in the 19th percentile – i.e., 19% 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 280,401 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 31st percentile – i.e., 31% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 38 others from the same source and published within six weeks on either side of this one. This one is in the 18th percentile – i.e., 18% of its contemporaries scored the same or lower than it.