Abstract
Cancer stem cells (CSCs), a subpopulation of cancer cells with ability of initiating tumorigenesis, exist in many kinds of tumors including breast cancer. Cancer stem cells contribute to treatment resistance and relapse. Conventional treatments only kill differentiated cancer cells, but spare CSCs. Combining conventional treatments with therapeutic drugs targeting to CSCs will eradicate cancer cells more efficiently. Studying the molecular mechanisms of CSCs regulation is essential for developing new therapeutic strategies. Growing evidences showed CSCs are regulated by non-coding RNA (ncRNA) including microRNAs and long non-coding RNAs (lncRNAs), and histone-modifiers, such as let-7, miR-93, miR-100, HOTAIR, Bmi-1 and EZH2. Herein we review the roles of microRNAs, lncRNAs and histone-modifiers especially Polycomb family proteins in regulating breast cancer stem cells (BCSCs).
Highlights
The concept of cancer stem cells (CSCs) has been generally accepted since leukaemia cancer stem cells were discovered by John E
We have shown that let-7a is downregulated in mammosperes in comparison to differentiated cancer cells utilizing miRNA array analysis; let-7a is lower in breast cancer stem cells (BCSCs) marked by CD24−CD44+ than nonCD24−CD44+ cells, and let-7a overexpression suppressed the mammosphere formation and tumor initiation
We mainly summarize the role of non-coding RNA (ncRNA) and histone-modifiers in regulating BCSCs
Summary
The concept of cancer stem cells (CSCs) has been generally accepted since leukaemia cancer stem cells were discovered by John E. Constitutive activation of Wnt signaling caused by the mutation of tumor suppressor APC leads to breast cancer stem cell (BCSC) expansion. We have shown that let-7a is downregulated in mammosperes in comparison to differentiated cancer cells utilizing miRNA array analysis; let-7a is lower in BCSCs marked by CD24−CD44+ than nonCD24−CD44+ cells, and let-7a overexpression suppressed the mammosphere formation and tumor initiation. SET7/9 which catalyzes monomethylation of histone 3 catalyzes methylation of Lin28A at K135 to promote Lin accumulation in nucleus, and increases the stability and pri-let-7-binding ability of Lin (Kim et al, 2014), suggesting epigenetic proteins can regulate CSCs. miR-200 family, including miR-200a, miR-200b, miR200c, miR-141 and miR-429, are reported as tumor suppressors.
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