Pro-senescence therapy for cancer treatment
Abstract
Abundant evidence points to a crucial physiological role for cellular senescence in combating tumorigenesis. Thus, the engagement of senescence may represent a key component for therapeutic intervention in the eradication of cancer. In this Opinion article, we focus on concepts that are relevant to a pro-senescence approach to therapy and we propose potential therapeutic strategies that aim to enhance the pro-senescence response in tumours.
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Pten heterozygosity promotes tumour initiation and proliferation in the prostate, but complete loss of Pten can oppose prostate tumorigenesis by triggering a powerful p53-dependent cellular senescence response.
“Pten heterozygosity promotes tumour initiation and proliferation in the prostate, but paradoxically, the complete loss of Pten can oppose prostate tumorigenesis by triggering a powerful p53-dependent cellular senescence response 38”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [38]
Methods that restore these p53-mediated functions might be fruitful in enhancing NK cell-mediated tumor elimination.
“Methods that restore these p53-mediated functions might therefore be fruitful in enhancing NK cell–mediated tumor elimination (Nardella et al., 2011).”
From p53-dependent chemokine production by senescent tumor cells supports NKG2D-dependent tumor elimination by natural killer cells (2013) · cites this paper as Nardella et al., 2011
The main advantage of the senescence response caused by traditional chemotherapeutic agents is that cancer cell senescence can be induced with lower doses than those used to cause cancer cell death, thus possibly reducing adverse side effects.
“The main advantage of the senescence response caused by traditional chemotherapeutic agents is that cancer cell senescence can be induced with lower doses than those used to cause cancer cell death, thus possibly reducing the adverse side effects [363,367].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [367]
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- Authors
- Nardella, C., Clohessy, J. G., Alimonti, A., & Pandolfi, P. P.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Pandolfi, Pier Paolo
- Venue
- Nature Reviews Cancer
- Published
- 2011-06-24
- Volume
- 11
- Issue
- 7
- Pages
- 503-511
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W2011997876
- Cited by
- 437
- References
- 33
- Citations by year
- 2026: 5 · 2025: 20 · 2024: 15 · 2023: 15 · 2022: 20 · 2021: 38 · 2020: 30 · 2019: 35 · 2018: 25 · 2017: 34 · 2016: 35 · 2015: 26 · 2014: 45 · 2013: 43 · 2012: 38
- FWCI
- 4.76
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System (Università degli Studi di Trento) (submittedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion)
- Funders
- Prostate Cancer Foundation
- National Institutes of Health (5u01ca141496-05)
- National Cancer Institute (U01-CA 141496, R01CA082328)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- cellular senescence, senescence induction, tumor suppression, carcinogenesis, cancer therapy, senolytics
- MeSH terms
- Cell Cycle, Humans, Neoplasms, Neoplastic Stem Cells, Tumor Suppressor Protein p53, Genes, myc, Cellular Senescence, PTEN Phosphohydrolase
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