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Adiponectin inhibits VEGF-A in prostate cancer cells

Overview of attention for article published in Tumor Biology, January 2015
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Mentioned by

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1 X user

Citations

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23 Mendeley
Title
Adiponectin inhibits VEGF-A in prostate cancer cells
Published in
Tumor Biology, January 2015
DOI 10.1007/s13277-015-3067-1
Pubmed ID
Authors

Qiruo Gao, Junhua Zheng, Xudong Yao, Bo Peng

Abstract

A role of adiponectin in tumorigenesis has recently been appreciated. Although plasma adiponectin levels in subjects with prostate cancer have been found to be significantly lower than in subjects with benign prostatic hyperplasia or in normal healthy controls, the underlying molecular mechanisms remain unknown. Here, we not only detected significant decreases in plasma adiponectin levels in prostate cancer patients, but also showed significant decreases in adiponectin receptor I (AdipoR1) levels in the resected prostate cancer specimen. Prostate cancer cell lines examined in the current study had all lower levels of adiponectin and AdipoR1, compared to normal healthy prostate tissue. Moreover, overexpression of adiponectin in prostate cancer cells decreased production of vascular endothelial growth factor A (VEGF-A), while adiponectin depletion increased VEGF-A. Furthermore, adiponectin seemed to activate AMPK/TSC2 to inhibit mTor-mediated activation of VEGF-A. Taken together, our data suggest that adiponectin may play an essential role in suppressing growth of prostate cancer cells through inhibition of VEGF-A-mediated cancer neovascularization.

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 23 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
France 1 4%
Unknown 22 96%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 5 22%
Student > Master 4 17%
Student > Ph. D. Student 3 13%
Student > Doctoral Student 2 9%
Other 2 9%
Other 1 4%
Unknown 6 26%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 22%
Agricultural and Biological Sciences 5 22%
Veterinary Science and Veterinary Medicine 2 9%
Medicine and Dentistry 2 9%
Immunology and Microbiology 1 4%
Other 3 13%
Unknown 5 22%
Attention Score in Context

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 22 January 2015.
All research outputs
#18,389,490
of 22,778,347 outputs
Outputs from Tumor Biology
#1,370
of 2,622 outputs
Outputs of similar age
#275,747
of 379,772 outputs
Outputs of similar age from Tumor Biology
#80
of 165 outputs
Altmetric has tracked 22,778,347 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,622 research outputs from this source. They receive a mean Attention Score of 2.2. This one is in the 30th percentile – i.e., 30% 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 379,772 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 16th percentile – i.e., 16% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 165 others from the same source and published within six weeks on either side of this one. This one is in the 37th percentile – i.e., 37% of its contemporaries scored the same or lower than it.