Short Telomeres Limit Tumor Progression In Vivo by Inducing Senescence
Open accessAbstract
Telomere maintenance is critical for cancer progression. To examine mechanisms of tumor suppression induced by short telomeres, we crossed mice deficient for the RNA component of telomerase, mTR(-/-), with Emu-myc transgenic mice, an established model of Burkitt's lymphoma. Short telomeres suppressed tumor formation in Emu-myc transgenic animals. Expression of Bcl2 blocked apoptosis in tumor cells, but surprisingly, mice with short telomeres were still resistant to tumor formation. Staining for markers of cellular senescence showed that pretumor cells induced senescence in response to short telomeres. Loss of p53 abrogated the short telomere response. This study provides in vivo evidence for the existence of a p53-mediated senescence mechanism in response to short telomeres that suppresses tumorigenesis.
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Crosses of telomerase-deficient mice with tumour model mice show that critically short telomeres limit tumour formation when the p53 pathway is functional.
“Crosses of telomerase-deficient mice with various tumour model mice have demonstrated that critically short telomeres limit tumour formation when the p53 pathway is functional51–55.”
From Telomeres in cancer: tumour suppression and genome instability (2017) · cites this paper as [55]
Telomere attrition-induced senescence is implicated in these tumour suppressive effects.
“telomere attrition-induced senescence is implicated in these tumour suppressive effects 17 .”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [17]
In a chemical carcinogenesis model, DMBA and phorbol esters induce skin papillomas by causing activating H-RAS mutations.
“application of 7,12-dimethylbenz(a)anthracene (DMBA) and phorbol esters 12-O-tetradecanoylphorbol 13-acetate induces high rates of skin papilloma formation by inducing activating mutations in the H-RAS gene (91).”
From Telomeres and telomerase in cancer (2010) · cites this paper as [91]
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References 41 · Cited by 314
Research works printed but not linked: 3
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- Authors
- Feldser, D. M., & Greider, C. W.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Greider, Carol W.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2007-05
- Volume
- 11
- Issue
- 5
- Pages
- 461-469
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC1945093
- OpenAlex
- W2145357417
- Cited by
- 314
- References
- 41
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 7 · 2023: 2 · 2022: 7 · 2021: 9 · 2020: 14 · 2019: 13 · 2018: 10 · 2017: 12 · 2016: 13 · 2015: 16 · 2014: 14 · 2013: 23 · 2012: 24
- FWCI
- 23.67
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (P01CA016519, P01CA013106)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- short telomeres, cellular senescence, tumor suppression, telomerase RNA, Eμ-myc transgenic mice, Burkitt lymphoma, Bcl-2, apoptosis, p53, telomere maintenance, carcinogenesis
- MeSH terms
- Animals, Burkitt Lymphoma, Mice, Transgenic, Genes, p53, Genes, myc, Telomere, Cellular Senescence, Disease Progression, Mice
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