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Role of estrogen in lung cancer based on the estrogen receptor-epithelial mesenchymal transduction signaling pathways

Overview of attention for article published in OncoTargets and therapy, October 2015
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Title
Role of estrogen in lung cancer based on the estrogen receptor-epithelial mesenchymal transduction signaling pathways
Published in
OncoTargets and therapy, October 2015
DOI 10.2147/ott.s90085
Pubmed ID
Authors

Xiao-zhen Zhao, Yu Liu, Li-juan Zhou, Xiao-yuan Yang, Zhong-qi Wang, Zhong-hua Wu

Abstract

Estrogen is reported to promote the occurrence and development of several human cancers. Increasing evidence shows that most human lung tumors exert estrogen receptor expression. In the present study, we investigated the underlying mechanism of estrogen effect in lung cancer through estrogen receptor-epithelial-mesechymal-transition signaling pathways for the first time. A total of 36 inbred C57BL/6 mice (18 male and 18 female) were injected subcutaneously with human lung adenocarcinoma cell line, Lewis. After the lung tumor model was established, mice with lung adenocarcinoma were randomly divided into three groups for each sex (n=6), such as vehicle group, estrogen group, and estrogen plus tamoxifen group. The six groups of mice were sacrificed after 21 days of drug treatment. Tumor tissue was stripped and weighed, and tumor inhibition rate was calculated based on average tumor weight. Protein and messenger RNA (mRNA) expressions of estrogen receptor α (ERα), estrogen receptor β (ERβ), phosphatidylinositol 3'-kinase (PI3K), AKT, E-cadherin, and vimentin were detected in both tumor tissue and lung tissue by using immunohistochemistry and real-time reverse transcription-polymerase chain reaction. 1) For male mice: in the estrogen group, estrogen treatment significantly increased ERα protein and mRNA expressions in tumor tissue and protein expression of PI3K, AKT, and vimentin in both tumor tissue and lung tissue compared with the vehicle-treated group. Besides, mRNA expression of E-cadherin was significantly reduced in estrogen-treated tumor tissues than that in vehicle-treated tissues. In the estrogen plus tamoxifen group, protein and mRNA expressions of ERα and AKT were dramatically reduced by tamoxifen treatment in tumor tissue compared with the estrogen group; mRNA expression of E-cadherin was increased in tumor tissue; protein expression of vimentin and PI3K were downregulated in tumor tissue; protein expression of E-cadherin increased in lung tissue; protein expression of ERα and PI3K were downregulated in lung tissue compared with the estrogen group. 2) For female mice: in the estrogen group, estrogen treatment significantly increased mRNA expression of ERβ and PI3K, and protein expression of ERβ, PI3K, AKT, and vimentin in both tumor tissue and lung tissue compared with the vehicle-treated group. mRNA expression of E-cadherin was downregulated in tumor tissue, and mRNA expression of AKT was increased in lung tissues compared with the vehicle-treated group. In the estrogen plus tamoxifen group, tamoxifen treatment dramatically reduced protein expression of ERα, ERβ, AKT, and vimentin but significantly increased protein expression of E-cadherin in tumor tissues and lung tissue compared with the estrogen group. mRNA expression of ERβ, PI3K, and AKT was dramatically reduced by tamoxifen treatment in lung tissues compared with the estrogen group. Estrogen promoted lung adenocarcinoma cell metastasis by inducing lung epithelial mesenchymal cells and reducing intercellular adhesion force through PI3K/AKT signaling pathway.

Mendeley readers

The data shown below were compiled from readership statistics for 12 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 12 100%

Demographic breakdown

Readers by professional status Count As %
Unspecified 4 33%
Student > Bachelor 4 33%
Other 1 8%
Student > Ph. D. Student 1 8%
Student > Doctoral Student 1 8%
Other 1 8%
Readers by discipline Count As %
Unspecified 4 33%
Pharmacology, Toxicology and Pharmaceutical Science 3 25%
Medicine and Dentistry 3 25%
Neuroscience 1 8%
Biochemistry, Genetics and Molecular Biology 1 8%
Other 0 0%

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 12 October 2015.
All research outputs
#11,265,921
of 12,661,434 outputs
Outputs from OncoTargets and therapy
#1,111
of 1,597 outputs
Outputs of similar age
#224,911
of 263,635 outputs
Outputs of similar age from OncoTargets and therapy
#46
of 51 outputs
Altmetric has tracked 12,661,434 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,597 research outputs from this source. They receive a mean Attention Score of 2.3. This one is in the 1st percentile – i.e., 1% 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 263,635 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 51 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.