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Review
. 2012 Feb 1;72(3):576-80.
doi: 10.1158/0008-5472.CAN-11-3070.

Cancer stem cells: distinct entities or dynamically regulated phenotypes?

Yunqing Li  1 , John Laterra
Affiliations
Review

Cancer stem cells: distinct entities or dynamically regulated phenotypes?

Yunqing Li et al. Cancer Res. .

Abstract

The origins of tumor-propagating neoplastic stem-like cells [cancer stem cells (CSC)] and their relationship to the bulk population of tumor cells that lack stem-like tumor-propagating features (i.e., transit-amplifying cancer progenitor cells) remain unclear. Recent findings from multiple laboratories show that cancer progenitor cells have the capacity to dedifferentiate and acquire a stem-like phenotype in response to either genetic manipulation or environmental cues. These findings suggest that CSCs and relatively differentiated progenitors coexist in dynamic equilibrium and are subject to bidirectional conversion. In this review, we discuss emerging concepts regarding the stem-like phenotype, its acquisition by cancer progenitor cells, and the molecular mechanisms involved. Understanding the dynamic equilibrium between CSCs and cancer progenitor cells is critical for the development of therapeutic strategies to deplete tumors of their tumor-propagating and treatment-resistant cell subpopulations.

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Figures

Figure 1
Figure 1
Transit-amplifying cancer progenitor cells acquire stem-like phenotypes by dedifferentiating mechanisms. A schematic model depicting the functional connections between microenvironmental signals, signal transduction pathways, and molecular circuitries including transcriptional networks, microRNAs, and epigenetic modifications induce dedifferentiation of cancer progenitor cells into CSC phenotypes. Transcriptional networks involving Oct4, Nanog and other transcription factors act as key inducers of dedifferentiation mechanisms.
See this image and copyright information in PMC

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