Abstract
Cancer stem cells (CSCs) are a small and elusive subpopulation of self-renewing cancer cells with remarkable ability to initiate, propagate, and spread the malignant disease. In addition, they exhibit increased resistance to anticancer therapies, thereby contributing to disease relapse. CSCs are reported to be present in many tumor types such as melanoma, sarcoma, mammary tumors, colon cancer and other solid tumors. These cells from different tumors show unique energetic and metabolic pathways. For example, CSCs from one type of tumor may predominantly use aerobic glycolysis, while from another tumor type may utilize oxidative phosphorylation. Most commonly these cells use fatty acid oxidation and ketone bodies as the main source of energy production. CSCs have a remarkable ability to reprogram their metabolism in order to survive under adverse conditions such as hypoxia, acidosis, and starvation. There is increasing interest to identify molecular targets that can be utilized to kill CSCs and to control their growth. In this review, we discuss how an understanding of the unique metabolism of CSCs from different tumors can offer promising strategies for targeting CSCs and hence to prevent disease relapse and to treat the metastatic disease.
Highlights
Cancer is the result of the accumulation of genetic and epigenetic changes that eventually lead to uncontrolled cell growth and the gain of invasive functions by cancer cells
There is metabolic difference between Cancer Stem Cell (CSC) and normal stem cells and between CSCs and differentiated tumor cells, so further studies are warranted to elucidate the role of preferred energy metabolic process over other metabolic processes in a particular type of CSCs [119]. It has been reported in glioma cancer stem cell and progenitor cells that CSCs exhibit low glucose consumption, low lactate production, high ATP generation, and high mitochondrial oxidation for their energy demands than their differentiated glioma cell, suggesting oxidative phosphorylation (OxPhos) be the main source for metabolic and energy dependency
Besides aerobic glycolysis and tricarboxylic acid (TCA) cycle, the role of fatty acid oxidation (FAO) in satisfying energy demands, chemoand immune-resistance, stemness, and cancer progression could be demonstrated by analyzing the lipolytic phenotype of CSCs that ispredominantly dictated by the tumor microenvironment [191]
Summary
Cancer is the result of the accumulation of genetic and epigenetic changes that eventually lead to uncontrolled cell growth and the gain of invasive functions by cancer cells. These observations suggest that Wnt/β-catenin signaling has an important role in the development of tumorigenicity and stemness features of CSCs. we can conclude that EMT is a necessarily parallel path by multi-grades tumor cells or CSCs for cancer progression, and to acquire metastatic and stem cell-like properties.
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