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Regulation of self‐renewal in normal and cancer stem cells
Author(s) -
Verga Falzacappa Maria V.,
Ronchini Chiara,
Reavie Linsey B.,
Pelicci Pier G.
Publication year - 2012
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2012.08727.x
Subject(s) - cancer stem cell , stem cell , biology , cancer cell , cancer , cancer research , microbiology and biotechnology , computational biology , genetics
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.