Abstract
Mutations can confer a selective advantage on specific cells, enabling them to go through the multistep process that leads to malignant transformation. The cancer stem cell hypothesis postulates that only a small pool of low-cycling stem-like cells is necessary and sufficient to originate and develop the disease. Normal and cancer stem cells share important functional similarities such as 'self-renewal' and differentiation potential. However, normal and cancer stem cells have different biological behaviours, mainly because of a profound deregulation of self-renewal capability in cancer stem cells. Differences in mode of division, cell-cycle properties, replicative potential and handling of DNA damage, in addition to the activation/inactivation of cancer-specific molecular pathways confer on cancer stem cells a malignant phenotype. In the last decade, much effort has been devoted to unravel the complex dynamics underlying cancer stem cell-specific characteristics. However, further studies are required to identify cancer stem cell-specific markers and targets that can help to confirm the cancer stem cell hypothesis and develop novel cancer stem cell-based therapeutic approaches. It has been shown that only a small sub-population of cells, the cancer stem cells (CSCs), is necessary and sufficient to originate a tumour. We discuss how, compared to normal SCs, CSCs exhibit a profound de-regulation of their self-renewal capability, mainly due to differences in mode of division, cell-cycle properties, replicative potential and handling of DNA-damage.
Original language | English |
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Pages (from-to) | 3559-3572 |
Number of pages | 14 |
Journal | FEBS Journal |
Volume | 279 |
Issue number | 19 |
DOIs | |
Publication status | Published - Oct 2012 |
Keywords
- asymmetric division
- cancer stem cell
- cancer therapy
- DNA damage
- genomic instability
- p21
- p53
- self-renewal
- stem cell
- symmetric division
ASJC Scopus subject areas
- Biochemistry
- Cell Biology
- Molecular Biology