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Kang, Byoung Heon
Cancer Biology Lab.
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TRAP1 Inhibition Increases Glutamine Synthetase Activity in Glutamine Auxotrophic Non-small Cell Lung Cancer Cells

Author(s)
Vo, Vu T. A.Choi, Jong-WhanPhan, Ai N. H.Hua, Tuyen N. M.Kim, Min-KyuKang, Byoung HeonJung, Soon-HeeYong, Suk-JoongJeong, Yangsik
Issued Date
2018-04
DOI
10.21873/anticanres.12460
URI
https://scholarworks.unist.ac.kr/handle/201301/24124
Fulltext
http://ar.iiarjournals.org/content/38/4/2187.abstract
Citation
ANTICANCER RESEARCH, v.38, no.4, pp.2187 - 2193
Abstract
Background/Aim: Cancer cells are distinct in terms of glutamine dependence. Here we investigated the different susceptibility of glutamine-independent and glutamine-dependent non-small cell lung cancer (NSCLC) to treatment with tumor necrosis factor receptor-associated protein 1 (TRAP1) inhibitor gamitrinib-triphenylphosphonium (G-TPP). Materials and Methods: Cell viability and proliferation under glutamine deprivation and G-TPP treatment were determined by the MTT and colony-formation assays. Protein and mRNA expression were determined by western blot and quantitative polymerase chain reaction. Colorimetric-based assay was performed to check for glutamine synthetase (GS) activity. Results: NSCLC cells showed diverse adaptation under glutamine-depleted condition and were categorized into glutamine-independent and glutamine-dependent cells. Treatment with G-TPP particularly increased GS activity and induced cell death due to energy shortage indicated by phosphorylated AMP-activated protein kinase (AMPK) in glutamine-dependent cells. Conclusion: This finding provides better understanding of TRAP1-mediated glutamine metabolism through GS activity, and evidence that TRAP1 could be a promising therapeutic target for glutamine-addicted cancer.
Publisher
INT INST ANTICANCER RESEARCH
ISSN
0250-7005
Keyword (Author)
Glutamine metabolismTRAP1gamitrinib-triphenylphosphoniumglutamine synthetaselung cancer
Keyword
MITOCHONDRIAL HSP90METABOLISMTHERAPYEXPRESSIONNETWORKSPROTEINGROWTHNSCLC

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