Source:http://linkedlifedata.com/resource/pubmed/id/19799519
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2010-2-26
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| pubmed:abstractText |
Cancer cells are unequal in a tumor mass and in established cultures. This is attributable to cancer stem cells with the unique ability to self-renew and to generate differentiating progeny. This ability is controlled at the level of asymmetric division by mechanisms that are yet not well defined. We found that normal and cancer keratinocyte fate was linked to the asymmetric distribution of epidermal growth factor receptor (EGFR) during mitosis. Although essential for epithelial cell proliferation, differentiation, and survival, this receptor was not present on the surface of cells satisfying criteria for stem cells such as quiescence, competence to produce functionally distinct daughters, high proliferative and clonogenic potential, sphere formation ability, and expression of stem cell markers. In contrast, keratinocytes displaying EGFR acquired a more differentiated phenotype, suggesting that EGFR may be involved in a switch from stem to transient amplifying cell fate. This switch was associated with changes in the expression profile of cell cycle, survival, and mitochondria controlling proteins that varied between normal and cancer cells. In conclusion, it appears that an unequal distribution of EGFR at mitosis controls keratinocyte fate by balancing quiescence and cycling of EGFR(-) cells, clearly malfunctioning in cancer. We believe that our findings provide mechanistic insights into the development of resistance to anti-EGFR therapies.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
1557-8534
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
19
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
209-20
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| pubmed:meshHeading |
pubmed-meshheading:19799519-Antigens, CD44,
pubmed-meshheading:19799519-Antigens, CD95,
pubmed-meshheading:19799519-Blotting, Western,
pubmed-meshheading:19799519-Carcinoma, Basal Cell,
pubmed-meshheading:19799519-Carcinoma, Squamous Cell,
pubmed-meshheading:19799519-Cell Cycle,
pubmed-meshheading:19799519-Cell Differentiation,
pubmed-meshheading:19799519-Cell Line, Tumor,
pubmed-meshheading:19799519-Cell Proliferation,
pubmed-meshheading:19799519-Cell Survival,
pubmed-meshheading:19799519-Cells, Cultured,
pubmed-meshheading:19799519-Fluorescent Antibody Technique,
pubmed-meshheading:19799519-Humans,
pubmed-meshheading:19799519-Keratinocytes,
pubmed-meshheading:19799519-Receptor, Epidermal Growth Factor,
pubmed-meshheading:19799519-Skin Neoplasms,
pubmed-meshheading:19799519-Tumor Cells, Cultured
|
| pubmed:year |
2010
|
| pubmed:articleTitle |
Asymmetric distribution of epidermal growth factor receptor directs the fate of normal and cancer keratinocytes in vitro.
|
| pubmed:affiliation |
U837, JPA Research Center, Lille Cedex, France.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|