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Hypoxia-induced modulation of PTEN activity and EMT phenotypes in lung cancers

Overview of attention for article published in Cancer Cell International, April 2016
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Title
Hypoxia-induced modulation of PTEN activity and EMT phenotypes in lung cancers
Published in
Cancer Cell International, April 2016
DOI 10.1186/s12935-016-0308-3
Pubmed ID
Authors

Takashi Kohnoh, Naozumi Hashimoto, Akira Ando, Koji Sakamoto, Shinichi Miyazaki, Daisuke Aoyama, Masaaki Kusunose, Motohiro Kimura, Norihito Omote, Kazuyoshi Imaizumi, Tsutomu Kawabe, Yoshinori Hasegawa

Abstract

Persistent hypoxia stimulation, one of the most critical microenvironmental factors, accelerates the acquisition of epithelial-mesenchymal transition (EMT) phenotypes in lung cancer cells. Loss of phosphatase and tensin homologue deleted from chromosome 10 (PTEN) expression might accelerate the development of lung cancer in vivo. Recent studies suggest that tumor microenvironmental factors might modulate the PTEN activity though a decrease in total PTEN expression and an increase in phosphorylation of the PTEN C-terminus (p-PTEN), resulting in the acquisition of the EMT phenotypes. Nevertheless, it is not known whether persistent hypoxia can modulate PTEN phosphatase activity or whether hypoxia-induced EMT phenotypes are negatively regulated by the PTEN phosphatase activity. We aimed to investigate hypoxia-induced modulation of PTEN activity and EMT phenotypes in lung cancers. Western blotting was performed in five lung cancer cell lines to evaluate total PTEN expression levels and the PTEN activation. In a xenograft model of lung cancer cells with endogenous PTEN expression, the PTEN expression was evaluated by immunohistochemistry. To examine the effect of hypoxia on phenotypic alterations in lung cancer cells in vitro, the cells were cultured under hypoxia. The effect of unphosphorylated PTEN (PTEN4A) induction on hypoxia-induced EMT phenotypes was evaluated, by using a Dox-dependent gene expression system. Lung cancer cells involving the EMT phenotypes showed a decrease in total PTEN expression and an increase in p-PTEN. In a xenograft model, loss of PTEN expression was observed in the tumor lesions showing tissue hypoxia. Persistent hypoxia yielded an approximately eight-fold increase in the p-PTEN/PTEN ratio in vitro. PTEN4A did not affect stabilization of hypoxia-inducible factor 1α. PTEN4A blunted hypoxia-induced EMT via inhibition of β-catenin translocation into the cytoplasm and nucleus. Our study strengthens the therapeutic possibility that compensatory induction of unphosphorylated PTEN may inhibit the acquisition of EMT phenotypes in lung cancer cells under persistent hypoxia.

Twitter Demographics

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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 %
Unknown 23 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 30%
Student > Bachelor 5 22%
Student > Master 3 13%
Professor > Associate Professor 2 9%
Researcher 1 4%
Other 1 4%
Unknown 4 17%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 10 43%
Medicine and Dentistry 5 22%
Veterinary Science and Veterinary Medicine 1 4%
Agricultural and Biological Sciences 1 4%
Nursing and Health Professions 1 4%
Other 0 0%
Unknown 5 22%

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 21 April 2016.
All research outputs
#6,567,037
of 7,584,550 outputs
Outputs from Cancer Cell International
#244
of 301 outputs
Outputs of similar age
#224,770
of 267,865 outputs
Outputs of similar age from Cancer Cell International
#11
of 12 outputs
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So far Altmetric has tracked 301 research outputs from this source. They receive a mean Attention Score of 3.5. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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We're also able to compare this research output to 12 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.