Increased epidermal tumors and increased skin wound healing in transgenic mice overexpressing the catalytic subunit of telomerase, mTERT, in basal keratinocytes
Open accessAbstract
Telomerase transgenics are an important tool to assess the role of telomerase in cancer, as well as to evaluate the potential use of telomerase for gene therapy of age-associated diseases. Here, we have targeted the expression of the catalytic component of mouse telomerase, mTERT, to basal keratinocytes using the bovine keratin 5 promoter. These telomerase-transgenic mice are viable and show histologically normal stratified epithelia with high levels of telomerase activity and normal telomere length. Interestingly, the epidermis of these mice is highly responsive to the mitogenic effects of phorbol esters, and it is more susceptible than that of wild-type littermates to the development skin tumors upon chemical carcinogenesis. The epidermis of telomerase-transgenic mice also shows an increased wound-healing rate compared with wild-type littermates. These results suggest that, contrary to the general assumption, telomerase actively promotes proliferation in cells that have sufficiently long telomeres and unravel potential risks of gene therapy for age-associated diseases based on telomerase upregulation.
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Overexpression of mouse telomerase reverse transcriptase catalytic subunit induces a variety of malignancies.
“Overexpression of the mouse telomerase reverse transcriptase catalytic subunit (mTERTcs) has been shown to induce a variety of malignancies64–66.”
From Stem cell aging: mechanisms, regulators and therapeutic opportunities (2014) · cites this paper as [66]
The human genome is widely altered through gene copy number changes, and telomere shortening during tumorigenesis can serve as a key mutator mechanism.
“Together, these data indicate that the human genome is widely altered through changes in gene copy number and that telomere shortening during tumorigenesis can serve as a key mutator mechanism.”
From Telomeres and telomerase in cancer (2010) · cites this paper as [135]
Increased telomerase activity in two independent Tert transgenic mouse models seemed to increase susceptibility to tumour formation.
“One caveat to such an approach is the observation that increased telomerase activity in two independent Tert transgenic mouse models seemed to increase the susceptibility for tumour formation 66, 67 .”
From The common biology of cancer and ageing (2007) · cites this paper as [66]
TERT promotes tumor development even in settings of ample telomere reserve.
“Moreover, recent findings indicate that TERT promotes tumor development even in settings of ample telomere reserve, although the mechanisms underlying these telomere length-independent activities of TERT remain unclear9–13.”
From Conditional telomerase induction causes proliferation of hair follicle stem cells (2005) · cites this paper as [9]
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- Authors
- González‐Suárez, E., Samper, E., Ramírez, A., Flores, J. M., Martín‐Caballero, J., Jorcano, J. L., & Blasco, M. A.
- Affiliations
- Centro Nacional de Biotecnología (ES)
- Universidad Complutense de Madrid (ES)
- Venue
- The EMBO Journal
- Published
- 2001-06-01
- Volume
- 20
- Issue
- 11
- Pages
- 2619-2630
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC125492
- OpenAlex
- W1995925983
- Cited by
- 372
- References
- 50
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 6 · 2023: 8 · 2022: 5 · 2021: 16 · 2020: 9 · 2019: 9 · 2018: 10 · 2017: 8 · 2016: 12 · 2015: 11 · 2014: 13 · 2013: 15 · 2012: 27
- FWCI
- 18.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The EMBO Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- European Commission
- Swiss Bridge Foundation
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- telomerase, basal keratinocytes, keratin 5 promoter, epidermal tumors, skin wound healing, chemical carcinogenesis, phorbol ester, telomere length
- MeSH terms
- Animals, Cattle, DNA-Binding Proteins, Female, Gastric Mucosa, Hyperplasia, Keratins, Mice, Transgenic, Mouth Mucosa, Neoplasms, Experimental, Papilloma, RNA, Skin, Skin Neoplasms, Stomach, Tetradecanoylphorbol Acetate, Vagina, Wound Healing, 9,10-Dimethyl-1,2-benzanthracene, Genetic Therapy, Keratinocytes, Genes, p53, Telomere, Mice, Knockout, Telomerase, Catalytic Domain, Protein Subunits, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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