Abstract
Adult stem cells maintain tissue homeostasis by their ability to both self-renew and differentiate to distinct cell types. Multiple signaling pathways have been shown to play essential roles as extrinsic cues in maintaining adult stem cell identity and activity. Recent studies also show dynamic regulation by epigenetic mechanisms as intrinsic factors in multiple adult stem cell lineages. Emerging evidence demonstrates intimate crosstalk between these two mechanisms. Misregulation of adult stem cell activity could lead to tumorigenesis, and it has been proposed that cancer stem cells may be responsible for tumor growth and metastasis. However, it is unclear whether cancer stem cells share commonalities with normal adult stem cells. In this review, we will focus on recent discoveries of epigenetic regulation in multiple adult stem cell lineages. We will also discuss how epigenetic mechanisms regulate cancer stem cell activity and probe the common and different features between cancer stem cells and normal adult stem cells.
Highlights
Adult stem cells are defined as cells that have two central properties: self-renewal and differentiation
We further demonstrate that both asymmetric histone 3 (H3) segregation during germline stem cells (GSCs) mitosis and post-mitotic rapid turnover of preexisting H3 in GB contribute to this asymmetric H3 distribution
We further showed that dUTX maintains active transcription of an inhibitor of the JAK-STAT pathway encoded by Suppressor of cytokine signaling at 36E (Socs36E) gene
Summary
Adult stem cells are defined as cells that have two central properties: self-renewal and differentiation. It is remarkable that Egg regulates both GSC self-renewal and differentiation by having an opposite effect on the same signaling pathway in a cell type-specific manner [36] Another H3K9 methyltransferase in Drosophila, dG9a, is required for the formation of functional spectrosome, an organelle required for asymmetric divisions of female GSCs. As a result of spectrosomal dysfunction, germaria. Using ChIP with H3K27me antibodies, the authors found that EZH2controlled target genes are derepressed in Dnmt haploinsufficient mice These data suggest that the PcG complexes might cooperate with DNA methylation to regulate leukemia stem cell activity and tumor growth [106]. Knockdown of mixed-lineage leukemia 1 (MLL1), an H3K4me methyltransferase, inhibits expression of HIF2α and reduces glioma stem cell self-renewal and growth [118] These data suggest that epigenetic regulation of CSCs directly controls cancer initiation and growth. Knockdown of Lsd leads to growth inhibition of pluripotent tumor cells, such as in teratocarcinoma, embryonic carcinoma and seminoma [123]
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