BMB Reports 2018; 51(7): 319-326
Cancer stem cell metabolism: target for cancer therapy
Young Chan Chae1 & Jae Ho Kim2,3,*
1School of Life Science, Ulsan National Institute of Science and Technology (UNIST), Ulsan 44919, 2Department of Physiology, School of Medicine, Pusan National University, Yangsan 50621, 3Research Institute of Convergence Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan 50621, Korea
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Received: April 3, 2018; Published online: July 31, 2018.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

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Increasing evidence suggests that cancer stem cell (CSC) theory represents an important mechanism underlying the observed failure of existing therapeutic modalities to fully eradicate cancers. In addition to their more established role in maintaining minimal residual disease after treatment and forming the new bulk of the tumor, CSCs might also critically contribute to tumor recurrence and metastasis. For this reason, specific elimination of CSCs may thus represent one of the most important treatment strategies. Emerging evidence has shown that CSCs have a different metabolic phenotype to that of differentiated bulk tumor cells, and these specific metabolic activities directly participate in the process of CSC transformation or support the biological processes that enable tumor progression. Exploring the role of CSC metabolism and the mechanism of the metabolic plasticity of CSCs has become a major focus in current cancer research. The targeting of CSC metabolism may provide new effective therapies to reduce the risk of recurrence and metastasis. In this review, we summarize the most significant discoveries regarding the metabolism of CSCs and highlight recent approaches in targeting CSC metabolism.
Keywords: Cancer Metabolism, Cancer Stem Cell, Glycolysis, Mitochondria, OXPHOS
Fig. 1. Impact of CSCs on the effectiveness of anticancer therapy. CSCs are a small sub population of bulk tumor cells that are highly chemo-resistant and play a prominent role in tumor relapse. While conventional therapy results in a transient reduction in the tumor by killing non-stem cancer cells (differentiated cancer cells), the remaining CSCs can form recurring tumors, and metastasis is induced by the formation of a secondary colony in distant organs. The use of CSC-specific inhibitors would reduce therapy resistance and relapse, and prevent metastasis, with a loss of stem cell properties.

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Funding Information
  • Ulsan National Institute of Science and Technology(UNIST)
  • National Research Foundation of Korea(NRF)
      2014M3A9D8034459, NRF-2016R1D1A1B03935769
  • Ministry of Health and Welfare(Ministry of Health, Welfare and Family Affairs)


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