Abstract
A limited subset of human leukemia cells has a self-renewal capacity and can propagate leukemia upon their transplantation into animals, and therefore, are named as leukemia stem cells, in the early 1990’s. Subsequently, cell subpopulations with similar characteristics were detected in various kinds of solid cancers and were denoted as cancer stem cells. Cancer stem cells are presently presumed to be crucially involved in malignant progression of solid cancer: chemoresitance, radioresistance, immune evasion, and metastasis. On the contrary, less attention has been paid to cancer non-stem cell population, which comprise most cancer cells in cancer tissues, due to the lack of suitable markers to discriminate cancer non-stem cells from cancer stem cells. Chronic myeloid leukemia stem cells generate a larger number of morphologically distinct non-stem cells. Moreover, accumulating evidence indicates that poor prognosis is associated with the increases in these non-stem cells including basophils and megakaryocytes. We will discuss the potential roles of cancer non-stem cells in fostering tumor microenvironment, by illustrating the roles of chronic myeloid leukemia non-stem cells including basophils and megakaryocytes in the pathogenesis of chronic myeloid leukemia, a typical malignant disorder arising from leukemic stem cells.
Highlights
Pluripotent stem cells in embryo can self-renew and can generate all mature cell types in the body as their potency to self-renew progressively decreases [1]
IL-6-STAT3 pathway activation induced cancer-associated fibroblasts (CAFs) to generate microvesicles containing miR-221, which was horizontally transferred to breast cancer non-stem cells, thereby promoting their acquisition of Cancer stem cell (CSC)-like phenotypes, in combination with hormone therapy [39]
Increases in non-stem cells such as basophils and platelets are associated with poor prognosis of chronic myeloid leukemia (CML) patients and it is highly likely that leukemia non-stem cells such as basophils and megakaryocytes, a precursor of platelets, can contribute to CML pathogenesis and progression
Summary
Pluripotent stem cells in embryo can self-renew and can generate all mature cell types in the body as their potency to self-renew progressively decreases [1]. Oncogenic BCR-ABL can transform hematopoietic stem cells into LSCs, and eventually can induce CML. Accumulating evidence indicates that cancer non-stem cells can acquire CSC-like phenotypes under various conditions (Fig. 2).
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