Open Access
Oncotarget, volume 8, issue 51, pages 88670-88688
Anti-angiogenic drugs: direct anti-cancer agents with mitochondrial mechanisms of action
Quayle Lewis A.
1, 2
,
Pereira Maria J.
3
,
Scheper Gerjan
1
,
Wiltshire Tammy
1
,
Peake Ria E.
1
,
Hussain Issam
1
,
Rea Carol A.
1
,
Bates Timothy
1, 4, 5
1
School of Life Sciences, Joseph Banks Laboratories, University of Lincoln, Lincoln, LN6 7DL, U.K.
|
2
Department of Oncology and Metabolism, Medical School, University of Sheffield, Sheffield, S10 2RX, U.K.
|
3
School of Pharmacy, Joseph Banks Laboratories, University of Lincoln, Lincoln, LN6 7DL, U.K.
|
4
Drugs With A Difference Limited, BioCity Nottingham, Nottingham, NG1 1GF, U.K.
|
5
Marlin Therapeutics Limited, Nottingham Science Park, Nottingham, NG7 2RF, U.K.
|
Publication type: Journal Article
Publication date: 2017-09-13
PubMed ID:
29179466
Oncology
Abstract
Components of the mitochondrial electron transport chain have recently gained much interest as potential therapeutic targets. Since mitochondria are essential for the supply of energy that is required for both angiogenic and tumourigenic activity, targeting the mitochondria represents a promising potential therapeutic approach for treating cancer. Here we investigate the established anti-angiogenesis drugs combretastatin A4, thalidomide, OGT 2115 and tranilast that we hypothesise are able to exert a direct anti-cancer effect in the absence of vasculature by targeting the mitochondria. Drug cytotoxicity was measured using the MTT assay. Mitochondrial function was measured in intact isolated mitochondria using polarography, fluorimetry and enzymatic assays to measure mitochondrial oxygen consumption, membrane potential and complex I-IV activities respectively. Combretastatin A4, OGT 2115 and tranilast were both shown to decrease mitochondrial oxygen consumption. OGT 2115 and tranilast decreased mitochondrial membrane potential and reduced complex I activity while combretastatin A4 and thalidomide did not. OGT 2115 inhibited mitochondrial complex II-III activity while combretastatin A4, thalidomide and tranilast did not. Combretastatin A4, thalidomide and OGT 2115 induced bi-phasic concentration-dependent increases and decreases in mitochondrial complex IV activity while tranilast had no evident effect. These data demonstrate that combretastatin A4, thalidomide, OGT 2115 and tranilast are all mitochondrial modulators. OGT 2115 and tranilast are both mitochondrial inhibitors capable of eliciting concentration-dependent reductions in cell viability by decreasing mitochondrial membrane potential and oxygen consumption.
Citations by journals
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1
2
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Biomedicine and Pharmacotherapy
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2 publications, 16.67%
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1 publication, 8.33%
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Future Oncology
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Future Oncology
1 publication, 8.33%
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Molecules
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Molecules
1 publication, 8.33%
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Clinical and Experimental Metastasis
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Clinical and Experimental Metastasis
1 publication, 8.33%
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Materials Research Express
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Materials Research Express
1 publication, 8.33%
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Biochemistry and Biophysics Reports
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Biochemistry and Biophysics Reports
1 publication, 8.33%
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Bioorganic Chemistry
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Bioorganic Chemistry
1 publication, 8.33%
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Pharmacology and Therapeutics
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Pharmacology and Therapeutics
1 publication, 8.33%
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1
2
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Citations by publishers
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1
2
3
4
5
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Elsevier
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Elsevier
5 publications, 41.67%
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Wiley
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Wiley
1 publication, 8.33%
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Future Medicine
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Future Medicine
1 publication, 8.33%
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Multidisciplinary Digital Publishing Institute (MDPI)
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Multidisciplinary Digital Publishing Institute (MDPI)
1 publication, 8.33%
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Springer Nature
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Springer Nature
1 publication, 8.33%
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IOP Publishing
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IOP Publishing
1 publication, 8.33%
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1
2
3
4
5
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- We do not take into account publications that without a DOI.
- Statistics recalculated only for publications connected to researchers, organizations and labs registered on the platform.
- Statistics recalculated weekly.
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Quayle L. A. et al. Anti-angiogenic drugs: direct anti-cancer agents with mitochondrial mechanisms of action // Oncotarget. 2017. Vol. 8. No. 51. pp. 88670-88688.
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Quayle L. A., Pereira M. J., Scheper G., Wiltshire T., Peake R. E., Hussain I., Rea C. A., Bates T. Anti-angiogenic drugs: direct anti-cancer agents with mitochondrial mechanisms of action // Oncotarget. 2017. Vol. 8. No. 51. pp. 88670-88688.
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TY - JOUR
DO - 10.18632/oncotarget.20858
UR - https://doi.org/10.18632%2Foncotarget.20858
TI - Anti-angiogenic drugs: direct anti-cancer agents with mitochondrial mechanisms of action
T2 - Oncotarget
AU - Quayle, Lewis A.
AU - Pereira, Maria J.
AU - Scheper, Gerjan
AU - Wiltshire, Tammy
AU - Peake, Ria E.
AU - Hussain, Issam
AU - Rea, Carol A.
AU - Bates, Timothy
PY - 2017
DA - 2017/09/13 00:00:00
PB - Impact Journals
SP - 88670-88688
IS - 51
VL - 8
PMID - 29179466
SN - 1949-2553
ER -
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@article{2017_Quayle,
author = {Lewis A. Quayle and Maria J. Pereira and Gerjan Scheper and Tammy Wiltshire and Ria E. Peake and Issam Hussain and Carol A. Rea and Timothy Bates},
title = {Anti-angiogenic drugs: direct anti-cancer agents with mitochondrial mechanisms of action},
journal = {Oncotarget},
year = {2017},
volume = {8},
publisher = {Impact Journals},
month = {sep},
url = {https://doi.org/10.18632%2Foncotarget.20858},
number = {51},
pages = {88670--88688},
doi = {10.18632/oncotarget.20858}
}
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Quayle, Lewis A., et al. “Anti-angiogenic drugs: direct anti-cancer agents with mitochondrial mechanisms of action.” Oncotarget, vol. 8, no. 51, Sep. 2017, pp. 88670-88688. https://doi.org/10.18632%2Foncotarget.20858.