Telomerase expression in human somatic cells does not induce changes associated with a transformed phenotype
- 1 January 1999
- journal article
- research article
- Published by Springer Nature in Nature Genetics
- Vol. 21 (1) , 111-114
- https://doi.org/10.1038/5056
Abstract
Expression of the human telomerase catalytic component, hTERT, in normal human somatic cells can reconstitute telomerase activity and extend their replicative lifespan1,2. We report here that at twice the normal number of population doublings, telomerase-expressing human skin fibroblasts (BJ-hTERT) and retinal pigment epithelial cells (RPE-hTERT) retain normal growth control in response to serum deprivation, high cell density, G1 or G2 phase blockers and spindle inhibitors. In addition, we observed no cell growth in soft agar and detected no tumour formation in vivo. Thus, we find that telomerase expression in normal cells does not appear to induce changes associated with a malignant phenotype.Keywords
This publication has 20 references indexed in Scilit:
- Extension of Life-Span by Introduction of Telomerase into Normal Human CellsScience, 1998
- Reconstitution of human telomerase with the template RNA component hTR and the catalytic protein subunit hTRTNature Genetics, 1997
- Involvement of the cyclin-dependent kinase inhibitor p16 (INK4a) in replicative senescence of normal human fibroblastsProceedings of the National Academy of Sciences, 1996
- A reversible, p53-dependent G0/G1 cell cycle arrest induced by ribonucleotide depletion in the absence of detectable DNA damage.Genes & Development, 1996
- The retinoblastoma protein and cell cycle controlCell, 1995
- Separation of Phenotypically Distinct Subpopulations of Cultured Human Retinal Pigment Epithelial CellsExperimental Cell Research, 1994
- Differential disruption of genomic integrity and cell cycle regulation in normal human fibroblasts by the HPV oncoproteins.Genes & Development, 1994
- Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53Published by Elsevier ,1992
- Wild-type p53 restores cell cycle control and inhibits gene amplification in cells with mutant p53 allelesCell, 1992
- Synchronization of HeLa cell cultures by inhibition of DNA polymerase a with aphidicolinNucleic Acids Research, 1980