Inactivation of p53 and life span extension of human diploid fibroblasts by mot-2

Normal human lung fibroblasts were transfected with expression plasmids encoding mot-2, an hsp70 family member that is associated with the immortal phenotype. After the empty vector-transfected controls had become senescent and positive for senescence-associated β-galactosidase (SA-β-gal), the mot-2...

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Bibliographic Details
Published in:FEBS letters 2000-06, Vol.474 (2), p.159-164
Main Authors: Kaul, Sunil C., Reddel, Roger R., Sugihara, Takashi, Mitsui, Youji, Wadhwa, Renu
Format: Article
Language:English
Subjects:
beta-Galactosidase - metabolism
Cell Division
Cell Line
Cell Size
Cellular Senescence
Diploidy
Fibroblasts - cytology
Fibroblasts - enzymology
Fibroblasts - metabolism
Half-Life
HSP70 Heat-Shock Proteins - genetics
HSP70 Heat-Shock Proteins - metabolism
Humans
Life span extension
Lung
Mitochondrial Proteins
mot-2
Normal human diploid fibroblast
Senescence
Transcription, Genetic - genetics
Transfection
Tumor suppressor p53
Tumor Suppressor Protein p53 - antagonists & inhibitors
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
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Summary:Normal human lung fibroblasts were transfected with expression plasmids encoding mot-2, an hsp70 family member that is associated with the immortal phenotype. After the empty vector-transfected controls had become senescent and positive for senescence-associated β-galactosidase (SA-β-gal), the mot-2-expressing cells continued to proliferate for an additional 12–18 population doublings and showed a young cell morphology and much lower SA-β-gal activity. The tumor suppressor p53 was found to be transcriptionally inactivated in life span-extended cells. We have thus shown for the first time that overexpression of mot-2 in normal human cells is able to permit their temporary escape from senescence.
ISSN:0014-5793
1873-3468
DOI:10.1016/S0014-5793(00)01594-5