Abstract
AbstractThe maintenance of stemness of normal stem cell is a complex process, where transcription factors like Oct-4, Bmi-1, and signaling pathways such as Wnt/β-catenin play important roles. This molecular set of mechanisms not only expands the population (self-renewal) but also keeps stem cells in a state of “de-differentiation.” Thus, stemness and differentiation are mutually exclusive and tightly regulated, where the idea of variation of stemness over time has not been incorporated. However, unlike normal stem cell stemness, tumor stemness may not be tightly regulated, where complexity of tumor microenvironment, especially hypoxic stress may allow for variation in stemness.In this review, we discuss the stem cell model of tumor growth and the emerging concept of tumor stemness. We also discuss our findings on the expansion of tumor stem cell–like side-population cells following hypoxic and drug-induced stress. We then propose a model of stemness switch, where quiescent TSCs (tumor stem cells) switch to a state of active and self-renewing TSC following stress.KeywordsTumor stemnessOxidative stressHypoxiaTumor stem cellTumor stem cell niche
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