Metabostemness in cancer: Linking metaboloepigenetics and mitophagy in remodeling cancer stem cells

Cancer stem cells (CSCs) are rare populations of malignant cells with stem cell-like features of self-renewal, uninterrupted differentiation, tumorigenicity, and resistance to conventional therapeutic agents, and these cells have a decisive role in treatment failure and tumor relapse. The self-renew...

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Published in:Stem cell reviews and reports 2022, Vol.18 (1), p.198-213
Main Authors: Naik, Prajna Paramita, Panigrahi, Swagatika, Parida, Ratnakar, Praharaj, Prakash Priyadarshi, Bhol, Chandra Sekhar, Patil, Shankargouda, Manjunath, NML, Ghosh, Dipanjan, Patra, Samir Kumar, Bhutia, Sujit Kumar
Format: Article
Language:English
Subjects:
Autophagy
Biomedical and Life Sciences
Biomedical Engineering and Bioengineering
Cancer
Cell Biology
Cell differentiation
Cell Differentiation - physiology
Cell self-renewal
Chromatin
Epigenetics
Humans
Life Sciences
Metabolism
Metabolites
Mitochondria
Mitochondria - metabolism
Mitophagy
Mitophagy - genetics
Neoplasms - metabolism
Neoplastic Stem Cells - metabolism
Regenerative Medicine/Tissue Engineering
Stem Cells
Tumor cells
Tumorigenicity
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Summary:Cancer stem cells (CSCs) are rare populations of malignant cells with stem cell-like features of self-renewal, uninterrupted differentiation, tumorigenicity, and resistance to conventional therapeutic agents, and these cells have a decisive role in treatment failure and tumor relapse. The self-renewal potential of CSCs with atypical activation of developmental signaling pathways involves the maintenance of stemness to support cancer progression. The acquisition of stemness in CSCs has been accomplished through genetic and epigenetic rewiring following the metabolic switch. In this context, “metabostemness” denotes the metabolic parameters that essentially govern the epitranscriptional gene reprogramming mechanism to dedifferentiate tumor cells into CSCs. Several metabolites often referred to as oncometabolites can directly remodel chromatin structure and thereby influence the operation of epitranscriptional circuits. This integrated metaboloepigenetic dimension of CSCs favors the differentiated cells to move in dedifferentiated macrostates. Some metabolic events might perform as early drivers of epitranscriptional reprogramming; however, subsequent metabolic hits may govern the retention of stemness properties in the tumor mass. Interestingly, selective removal of mitochondria through autophagy can promote metabolic plasticity and alter metabolic states during differentiation and dedifferentiation. In this connection, novel metabostemness-specific drugs can be generated as potential cancer therapeutics to target the metaboloepigenetic circuitry to eliminate CSCs. Graphical abstract
ISSN:2629-3269
2629-3277
DOI:10.1007/s12015-021-10216-9