Restoration of the Cellular Senescence Program and Repression of Telomerase by Human Chromosome 3
- 1 October 1995
- journal article
- Published by Wiley in Japanese Journal of Cancer Research
- Vol. 86 (10) , 899-904
- https://doi.org/10.1111/j.1349-7006.1995.tb02998.x
Abstract
Telomeres, at the end of chromosomes, shorten with each cell division, resulting in cellular senescence. Tumor cells, unlike normal somatic cells, express a telomerase that maintains the telomere length. Deletion of a gene(s) on chromosome 3 is common in human renal cell carcinoma (RCC) and reintroduction of a normal chromosome 3 into an RCC immortal cell line restored the program of cellular senescence. The loss of indefinite growth potential was associated with the loss of telomerase activity and shortening of telomeres in the RCC cells with a normal chromosome 3. However, microcell hybrids that escaped from senescence and microcell hybrids with an introduced chromosome 7 or 11 maintained telomere lengths and telomerase activity similar to those of the parental RCC23. Thus, restoration of the cellular senescence program by chromosome 3 is associated with repression of telomerase function in RCC cells.Keywords
This publication has 26 references indexed in Scilit:
- Telomere end-replication problem and cell agingPublished by Elsevier ,2004
- The limited in vitro lifetime of human diploid cell strainsPublished by Elsevier ,2004
- The telomere hypothesis of cellular agingExperimental Gerontology, 1992
- Telomere positional effects and the regulation of cellular senescenceTrends in Genetics, 1992
- Senescence of Nickel-Transformed Cells by an X Chromosome: Possible Epigenetic ControlScience, 1991
- Replicative Senescence: the Human Fibroblast Comes of AgeScience, 1990
- Telomeres and Their SynthesisScience, 1990
- Telomeres shorten during ageing of human fibroblastsNature, 1990
- Induction of Cellular Senescence in Immortalized Cells by Human Chromosome 1Science, 1990
- Human telomeres: fusion and interstitial sitesTrends in Genetics, 1989