Abstract
Cancer cells usually proliferate by symmetric division, producing identical copies of themselves. However, a small subset of cancer cells, mainly cancer stem cells, are capable of asymmetric cell division (ACD), producing a self-renewing daughter cell and a more differentiated daughter cell. During division, symmetry is broken by the spatial imbalance of polarity proteins and cell fate determinants. Present in both prokaryotes and eukaryotes, ACD can help establish diversity and hierarchy in the cell population and stabilize the number of stem and progenitor cells and balance it with functional cells. Abolishment of ACD in favor of symmetric self-renewal generates hyperproliferative cancer precursors with aberrantly specified fate, although ACD could enhance tumor resistance to chemo- and radiation therapies by producing a reservoir of quiescent cells. This chapter reviews the regulation of ACD and the functional consequences of ACD disruption in a variety of cancers.
| Original language | English (US) |
|---|---|
| Title of host publication | Cancer Stem Cells |
| Subtitle of host publication | Targeting the Roots of Cancer, Seeds of Metastasis, and Sources of Therapy Resistance |
| Publisher | Elsevier Inc. |
| Pages | 285-315 |
| Number of pages | 31 |
| ISBN (Electronic) | 9780128039342 |
| ISBN (Print) | 9780128038925 |
| DOIs | |
| State | Published - Sep 1 2016 |
| Externally published | Yes |
Keywords
- Asymmetric division
- Cell fate determinant
- Notch signaling
- Numb
- PAR
- Polarity
ASJC Scopus subject areas
- General Biochemistry, Genetics and Molecular Biology
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