Abstract
The subpopulation of cancer stem cells (CSCs) within tumor bulk are known for tumor recurrence and metastasis. CSCs show intrinsic resistance to conventional therapies and phenotypic plasticity within the tumor, which make these a difficult target for conventional therapies. CSCs have different metabolic phenotypes based on their needs as compared to the bulk cancer cells. CSCs show metabolic plasticity and constantly alter their metabolic state between glycolysis and oxidative metabolism (OXPHOS) to adapt to scarcity of nutrients and therapeutic stress. The metabolic characteristics of CSCs are distinct compared to non-CSCs and thus provide an opportunity to devise more effective strategies to target CSCs. Mechanism for metabolic switch in CSCs is still unravelled, however existing evidence suggests that tumor microenvironment affects the metabolic phenotype of cancer cells. Understanding CSCs metabolism may help in discovering new and effective clinical targets to prevent cancer relapse and metastasis. This review summarises the current knowledge of CSCs metabolism and highlights the potential targeted treatment strategies.
Highlights
Cancer causes significant deaths worldwide, despite major innovations in treatment therapy strategies, radiation- and chemo-therapy and drug delivery technologies
A non-essential amino acid, glutamine becomes essential for cancer cells [76] and cancer stem cells (CSCs) from lung, pancreatic and ovarian cancer have shown glutamine dependence [77, 78]
Hematopoietic stem cells (HSCs) and leukemia-initiating cells depend on fatty acid oxidation (FAO) for self-renewal [95, 99] and FAO inhibition is a potential pharmacological opportunity to target CSCs [98]
Summary
Department of Biophysics, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India Reviewed by: Pritam Sadhukhan, Johns Hopkins University, United States Herbert Levine, Rice University, United States Specialty section: This article was submitted to Cancer Metabolism, a section of the journal
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