Tumour cell metabolism is very different from normal cell metabolism; cancer cells re-programme the metabolic pathways that occur in normal cells in such a manner that it optimizes their proliferation, growth and survival. Although this metabolic re-programming obviously operates to the advantage of the tumour, it also offers unique opportunities for effective cancer therapy. Molecules that target the tumour cell-specific metabolic pathways have potential as novel anti-cancer drugs. Lonidamine belongs to this group of molecules and is already in use in some countries for cancer treatment. It has been known for a long time that lonidamine interferes with energy production in tumour cells by inhibiting hexokinase II (HKII), a glycolytic enzyme. However, subsequent studies have uncovered additional pharmacological targets for the drug, which include the electron transport chain and the mitochondrial permeability transition pore, thus expanding the pharmacological effects of the drug on tumour cell metabolism. A study by Nancolas et al. in a recent issue of the Biochemical Journal identifies two additional new targets for lonidamine: the pyruvate transporter in the mitochondria and the H+-coupled monocarboxylate transporters in the plasma membrane (PM). It is thus becoming increasingly apparent that the anti-cancer effects of lonidamine do not occur through a single target; the drug works at multiple sites. Irrespective of the molecular targets, what lonidamine does in the end is to undo what the tumour cells have done in terms of re-programming cellular metabolism and mitochondrial function.
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June 2016
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Overnight culture of mutant (mlt1Δ/Δ) strain of Candida albicans, spotted on to BSA agar plate and grown at 30°C for 5 days. For further information please see pp. 1537–1552. Image kindly provided by Rajendra Prasad. - PDF Icon PDF LinkFront Matter
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May 27 2016
Re-programming tumour cell metabolism to treat cancer: no lone target for lonidamine
Yangzom D. Bhutia;
Yangzom D. Bhutia
*Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A.
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Ellappan Babu;
Ellappan Babu
*Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A.
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Vadivel Ganapathy
Vadivel Ganapathy
1
*Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A.
1To whom correspondence should be addressed (email vadivel.ganapathy@ttuhsc.edu).
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Publisher: Portland Press Ltd
Received:
February 04 2016
Revision Received:
February 18 2016
Accepted:
February 19 2016
Online ISSN: 1470-8728
Print ISSN: 0264-6021
© 2016 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society
2016
Biochem J (2016) 473 (11): 1503–1506.
Article history
Received:
February 04 2016
Revision Received:
February 18 2016
Accepted:
February 19 2016
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Citation
Yangzom D. Bhutia, Ellappan Babu, Vadivel Ganapathy; Re-programming tumour cell metabolism to treat cancer: no lone target for lonidamine. Biochem J 1 June 2016; 473 (11): 1503–1506. doi: https://doi.org/10.1042/BCJ20160068
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