Abstract
Cancerous tumours contain a rare subset of cells with stem‐like properties that are termed cancer stem cells (CSCs). CSCs are defined by their ability to divide both symmetrically and asymmetrically, to initiate new tumour growth and to tolerate the foreign niches required for metastatic dissemination. Accumulating evidence suggests that tumours arise from cells with stem‐like properties, the generation of CSCs is therefore likely to be an initiatory event in carcinogenesis. Furthermore, CSCs in established tumours exist in a dynamic and plastic state, with nonstem tumour cells thought to be capable of de‐differentiation to CSCs. The regulation of the CSC state both during tumour initiation and within established tumours is a desirable therapeutic target and is mediated by epigenetic factors. In this review, we will explore the epigenetic parallels between induced pluripotency and the generation of CSCs, and discuss how the epigenetic regulation of CSCs opens up novel opportunities for therapeutic intervention.
Highlights
As with adult tissues, cancerous tumours contain a rare subset of cells with stem-like properties that can function to regenerate the heterogeneous cell populations observed therein
Low let-7 expression allowed for elevated levels of IL6, which in turn reactivated NFkB. This epigenetic positive feedback loop was found to be essential for maintaining the transformed state of breast cancer cells.[128]. These findings strongly suggest that the Lin-28/ let-7 miRNA axis may control the generation of cancer stem cell (CSC) in cancer as it does with pluripotency of noncancerous cells
The epigenetic processes involved in CSC generation have substantial implications for tumour initiation, metastasis and relapse
Summary
Funding information Cancer Research UK, Grant/Award Number: C59392/A25064; Pancreatic Cancer UK, Grant/Award Number: 2018RIF_03
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