Prolonged unbalanced growth induces cellular senescence markers linked with mechano transduction in normal and tumor cells

Cellular senescence is induced by diverse means and hence thought to be mediated by multiple pathways. We show that prolonged unbalanced growth due to retardation of DNA replication elicits a senescence-like phenomenon irrespective of the cell type. In fact, modest inhibition of DNA replication by v...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2005-09, Vol.335 (2), p.558-565
Main Authors: Sumikawa, Emi, Matsumoto, Yuko, Sakemura, Risa, Fujii, Michihiko, Ayusawa, Dai
Format: Article
Language:English
Subjects:
Actins - chemistry
Apoptosis
beta-Galactosidase - metabolism
Biophysics - methods
Blotting, Northern
Blotting, Western
Cell Cycle
Cell Line
Cell Line, Tumor
Cell Proliferation
Cell Shape
Cell Size
Cell Survival
Cell swelling
Cellular Senescence
DNA - chemistry
DNA - metabolism
DNA Replication
Fibroblasts - metabolism
Flow Cytometry
Gene Expression Regulation
Gene Expression Regulation, Neoplastic
HeLa Cells
Humans
MAP kinase cascade
MAP Kinase Signaling System
Mechano transduction
Phenotype
Plasmids - metabolism
Time Factors
Unbalanced growth
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Summary:Cellular senescence is induced by diverse means and hence thought to be mediated by multiple pathways. We show that prolonged unbalanced growth due to retardation of DNA replication elicits a senescence-like phenomenon irrespective of the cell type. In fact, modest inhibition of DNA replication by various means led to cell swelling, cytoskeletal alterations, and irregularly enlarged, flat cell shape. Such cells upregulated senescence-associated genes, and eventually lost division potential. These phenotypes, which define cellular senescence, were virtually reversed by reducing protein synthesis or blocking ERK of the MAP kinase family. These results suggest that cellular senescence is a manifestation of prolonged unbalanced growth linked with mechano transduction and can be prevented by at least two different ways.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2005.07.106