Evidence of oncogene-induced senescence in thyroid carcinogenesis
Open accessAbstract
Oncogene-induced senescence (OIS) is a growth arrest triggered by the enforced expression of cancer-promoting genes and acts as a barrier against malignant transformation in vivo . In this study, by a combination of in vitro and in vivo approaches, we investigate the role of OIS in tumours originating from the thyroid epithelium. We found that expression of different thyroid tumour-associated oncogenes in primary human thyrocytes triggers senescence, as demonstrated by the presence of OIS hallmarks: changes in cell morphology, accumulation of SA-β-Gal and senescence-associated heterochromatic foci, and upregulation of transcription of the cyclin-dependent kinase inhibitors p16 INK4a and p21 CIP1 . Furthermore, immunohistochemical analysis of a panel of thyroid tumours characterised by different aggressiveness showed that the expression of OIS markers such as p16 INK4a , p21 CIP1 and IGFBP7 is upregulated at early stages, and lost during thyroid tumour progression. Taken together, our results suggest a role of OIS in thyroid carcinogenesis.
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Senescent cells can be found in both benign and malignant tumours.
“Supporting this notion, the burden of senescent cells in tissues increases significantly with age in mice, primates, and humans,27 and they can be found in both benign and malignant tumours.31–35”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [33]
Since senescent cells are generally abundant in benign tumours and also present at low numbers in several malignancies, their paracrine activities could contribute to tumour progression and cancer metastasis.
“Since senescent cells are generally abundant in benign tumours and also present at low numbers in several malignancies,31–34,57 their paracrine activities could contribute to tumour progression and cancer metastasis.”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [33]
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- Authors
- Vizioli, M. G., Possik, P. A., Tarantino, E., Meissl, K., Borrello, M. G., Miranda, C., Anania, M. C., Pagliardini, S., Seregni, E., Pierotti, M. A., Pilotti, S., Peeper, D. S., & Greco, A.
- Affiliations
- Fondazione IRCCS Istituto Nazionale dei Tumori (IT)
- The Netherlands Cancer Institute (NL)
- ORCID
- Venue
- Endocrine-Related Cancer
- Publisher
- Bioscientifica
- Published
- 2011-09-21
- Volume
- 18
- Issue
- 6
- Pages
- 743-757
- ISSN
- 1351-0088 (ISSN-L)
- 1479-6821
- OpenAlex
- W2097632521
- Cited by
- 47
- References
- 49
- Citations by year
- 2025: 2 · 2023: 3 · 2022: 4 · 2021: 3 · 2020: 3 · 2019: 7 · 2018: 4 · 2017: 5 · 2016: 2 · 2015: 2 · 2014: 6 · 2013: 4 · 2012: 2
- FWCI
- 2.62
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrine Related Cancer (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Associazione Italiana per la Ricerca sul Cancro (5 x mille)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- oncogene-induced senescence, thyroid carcinogenesis, thyroid tumors, thyroid follicular cells, p16INK4a, p21, IGFBP7, senescence-associated heterochromatin foci, SA-β-galactosidase, cyclin-dependent kinase inhibitors, tumor progression, malignant transformation
- MeSH terms
- Thyroid Cancer, Papillary, Adult, Aged, Aging, Carcinoma, Carcinoma, Papillary, Cells, Cultured, Female, Humans, Male, Middle Aged, Proto-Oncogenes, Thyroid Gland, Thyroid Neoplasms, Transduction, Genetic, Insulin-Like Growth Factor Binding Proteins, Cyclin-Dependent Kinase Inhibitor p16, Cyclin-Dependent Kinase Inhibitor p21, HEK293 Cells, Thyroid Carcinoma, Anaplastic
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