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KLF5 inhibits angiogenesis in PTEN-deficient prostate cancer by attenuating AKT activation and subsequent HIF1α accumulation

Overview of attention for article published in Molecular Cancer, April 2015
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Mentioned by

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3 tweeters

Citations

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28 Dimensions

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27 Mendeley
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Title
KLF5 inhibits angiogenesis in PTEN-deficient prostate cancer by attenuating AKT activation and subsequent HIF1α accumulation
Published in
Molecular Cancer, April 2015
DOI 10.1186/s12943-015-0365-6
Pubmed ID
Authors

Xinpei Ci, Changsheng Xing, Baotong Zhang, Zhiqian Zhang, Jenny Jianping Ni, Wei Zhou, Jin-Tang Dong

Abstract

KLF5 is a basic transcriptional factor that regulates multiple physiopathological processes. Our recent study showed that deletion of Klf5 in mouse prostate promotes tumorigenesis initiated by the deletion of Pten. While molecular characterization of Klf5-null tumors suggested that angiogenesis was partially responsible for tumor promotion, the precise function and mechanism of KLF5 deletion in prostate tumor angiogenesis remain unclear. Applying histological staining to Pten-null mouse prostates, we observed that deletion of Klf5 significantly increased the number of microvessels, accompanied by the upregulation of multiple angiogenesis-related genes based on microarray analysis with MetaCore software. In human umbilical vein endothelial cells (HuVECs), tube formation and migration, both of which are indicators of angiogenic activities, were decreased by conditioned media from PC-3 and DU 145 human prostate cancer cells with KLF5 overexpression, but increased by media from cells with KLF5 knockdown. HIF1α, a key angiogenesis inducer, was upregulated by KLF5 loss at the protein but not the mRNA level in both mouse tissues and human cell lines, as determined by immunohistochemical staining, real-time RT-PCR and Western blotting. Consistently, KLF5 loss also upregulated VEGF and PDGF, two pro-angiogenic mediators of HIF1α function, as analyzed by immunohistochemical staining in mouse tissues and ELISA in conditioned media. Mechanistically, AKT activity, which caused the accumulation of HIF1α, was increased by KLF5 knockout or knockdown but decreased by KLF5 overexpression. PI3K/AKT inhibitors consistently abolished the effects of KLF5 knockdown on angiogenic activity, HIF1α accumulation, and VEGF and PDGF expression. KLF5 loss enhances tumor angiogenesis by attenuating PI3K/AKT signaling and subsequent accumulation of HIF1α in PTEN deficient prostate tumors.

Twitter Demographics

The data shown below were collected from the profiles of 3 tweeters 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 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Japan 1 4%
Denmark 1 4%
Unknown 25 93%

Demographic breakdown

Readers by professional status Count As %
Student > Master 4 15%
Other 3 11%
Student > Bachelor 3 11%
Student > Ph. D. Student 3 11%
Lecturer 2 7%
Other 4 15%
Unknown 8 30%
Readers by discipline Count As %
Agricultural and Biological Sciences 7 26%
Biochemistry, Genetics and Molecular Biology 5 19%
Medicine and Dentistry 3 11%
Pharmacology, Toxicology and Pharmaceutical Science 2 7%
Unknown 10 37%

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 05 February 2016.
All research outputs
#3,339,167
of 7,103,144 outputs
Outputs from Molecular Cancer
#280
of 677 outputs
Outputs of similar age
#98,704
of 199,640 outputs
Outputs of similar age from Molecular Cancer
#17
of 36 outputs
Altmetric has tracked 7,103,144 research outputs across all sources so far. This one has received more attention than most of these and is in the 50th percentile.
So far Altmetric has tracked 677 research outputs from this source. They receive a mean Attention Score of 3.2. This one has gotten more attention than average, scoring higher than 51% of its peers.
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 199,640 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 46th percentile – i.e., 46% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 36 others from the same source and published within six weeks on either side of this one. This one is in the 44th percentile – i.e., 44% of its contemporaries scored the same or lower than it.