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Indoleamine-2,3-dioxygenase elevated in tumor-initiating cells is suppressed by mitocans

M. Stapelberg, R. Zobalova, MN. Nguyen, T. Walker, M. Stantic, J. Goodwin, EA. Pasdar, T. Thai, K. Prokopova, B. Yan, S. Hall, N. de Pennington, SR. Thomas, G. Grant, J. Stursa, M. Bajzikova, AC. Meedeniya, J. Truksa, SJ. Ralph, O. Ansorge, LF....

. 2014 ; 67 (-) : 41-50.

Language English Country United States

Document type Journal Article, Research Support, Non-U.S. Gov't

Persistent link   https://www.medvik.cz/link/bmc15014590

Tumor-initiating cells (TICs) often survive therapy and give rise to second-line tumors. We tested the plausibility of sphere cultures as models of TICs. Microarray data and microRNA data analysis confirmed the validity of spheres as models of TICs for breast and prostate cancer as well as mesothelioma cell lines. Microarray data analysis revealed the Trp pathway as the only pathway upregulated significantly in all types of studied TICs, with increased levels of indoleamine-2,3-dioxygenase-1 (IDO1), the rate-limiting enzyme of Trp metabolism along the kynurenine pathway. All types of TICs also expressed higher levels of the Trp uptake system consisting of CD98 and LAT1 with functional consequences. IDO1 expression was regulated via both transcriptional and posttranscriptional mechanisms, depending on the cancer type. Serial transplantation of TICs in mice resulted in gradually increased IDO1. Mitocans, represented by α-tocopheryl succinate and mitochondrially targeted vitamin E succinate (MitoVES), suppressed IDO1 in TICs. MitoVES suppressed IDO1 in TICs with functional mitochondrial complex II, involving transcriptional and posttranscriptional mechanisms. IDO1 increase and its suppression by VE analogues were replicated in TICs from primary human glioblastomas. Our work indicates that IDO1 is increased in TICs and that mitocans suppress the protein.

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$a Tumor-initiating cells (TICs) often survive therapy and give rise to second-line tumors. We tested the plausibility of sphere cultures as models of TICs. Microarray data and microRNA data analysis confirmed the validity of spheres as models of TICs for breast and prostate cancer as well as mesothelioma cell lines. Microarray data analysis revealed the Trp pathway as the only pathway upregulated significantly in all types of studied TICs, with increased levels of indoleamine-2,3-dioxygenase-1 (IDO1), the rate-limiting enzyme of Trp metabolism along the kynurenine pathway. All types of TICs also expressed higher levels of the Trp uptake system consisting of CD98 and LAT1 with functional consequences. IDO1 expression was regulated via both transcriptional and posttranscriptional mechanisms, depending on the cancer type. Serial transplantation of TICs in mice resulted in gradually increased IDO1. Mitocans, represented by α-tocopheryl succinate and mitochondrially targeted vitamin E succinate (MitoVES), suppressed IDO1 in TICs. MitoVES suppressed IDO1 in TICs with functional mitochondrial complex II, involving transcriptional and posttranscriptional mechanisms. IDO1 increase and its suppression by VE analogues were replicated in TICs from primary human glioblastomas. Our work indicates that IDO1 is increased in TICs and that mitocans suppress the protein.
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$a Zobalová, Renata $u School of Medical Science, Griffith Health Institute, Griffith University, Southport, 4222 QLD, Australia; Institute of Biotechnology, Academy of Sciences of the Czech Republic, Prague 142 20, Czech Republic. $7 xx0310352
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$a Nguyen, Maria Nga $u School of Medical Science, Griffith Health Institute, Griffith University, Southport, 4222 QLD, Australia.
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$a Walker, Tom $u School of Medical Science, Griffith Health Institute, Griffith University, Southport, 4222 QLD, Australia; Department of Neurosurgery, John Radcliffe Hospital, Oxford OX3 9DU, UK.
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$a Pasdar, Elham Alizadeh $u School of Medical Science, Griffith Health Institute, Griffith University, Southport, 4222 QLD, Australia.
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$a Thai, Thuan $u Centre for Vascular Research, School of Medical Sciences, University of New South Wales, Sydney, 2052 NSW, Australia.
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$a Prokopova, Katerina $u Institute of Biotechnology, Academy of Sciences of the Czech Republic, Prague 142 20, Czech Republic; Faculty of Science, Charles University, 11000 Prague 1, Czech Republic.
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$a Yan, Bing $u School of Medical Science, Griffith Health Institute, Griffith University, Southport, 4222 QLD, Australia.
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$a Hall, Susan $u School of Pharmacy, Griffith Health Institute, Griffith University, Southport, 4222 QLD, Australia.
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$a de Pennington, Nicholas $u Department of Neurosurgery, John Radcliffe Hospital, Oxford OX3 9DU, UK.
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$a Stursa, Jan $u School of Medical Science, Griffith Health Institute, Griffith University, Southport, 4222 QLD, Australia; Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, Prague 160 00, Czech Republic.
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$a Bajzikova, Martina $u Institute of Biotechnology, Academy of Sciences of the Czech Republic, Prague 142 20, Czech Republic.
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$a Truksa, Jaroslav $u Institute of Biotechnology, Academy of Sciences of the Czech Republic, Prague 142 20, Czech Republic.
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$a Ralph, Stephen J $u School of Medical Science, Griffith Health Institute, Griffith University, Southport, 4222 QLD, Australia.
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