Senescence in polyploid giant cancer cells: A road that leads to chemoresistance
Abstract
Cellular senescence has been associated with age-related diseases, wound healing, fibrosis, diabetes and cancer. Senescent cells lack the capacity to proliferate, but are known to aggravate tumorigenesis. The polyploid giant cells arise from the cancer cell population mainly due to genotoxic stress caused by chemotherapy and/or radiotherapy. They exhibit features of senescence and have been reported to secrete an array of cytokines, chemokines and growth factors. These small molecules can bind to their receptors located on the surface of neighboring cells and activate/deactivate relevant signaling pathways, thereby modulating the tumor microenvironment. Some of these signaling cascade(s) might play a role in imparting therapy resistance to the cancer cells. This review throws light on the incidence of senescence and how the senescent polyploid giant cells affect the tumor microenvironment. Their role in giving rise to chemoresistant cancer cell population as well as acquired chemoresistance in the neighboring cancer cells along with various potential and established therapeutic avenues have also been discussed.
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Senescence may provide a pathway for disease recurrence after cancer therapy.
“and may provide a pathway for disease recurrence after cancer therapy.”
From Senescence and Cancer: A Review of Clinical Implications of Senescence and Senotherapies (2020) · cites this paper as [21]
Radiotherapy and chemotherapy may trigger either cell death at high doses or senescence at non-lethal doses.
“There are also potential interactions with cancer therapies, in particular, radiotherapy and chemotherapy, which may trigger either cell death at high doses or senescence at non-lethal doses.”
From Senescence and Cancer: A Review of Clinical Implications of Senescence and Senotherapies (2020) · cites this paper as [21]
Some therapy-induced senescent cells may reactivate and lead to recurrence.
“This induced senescence may be viewed as a cytostatic clinical response, but some of these therapy induced senescent cells may reactivate and lead to recurrence [20,21,22].”
From Senescence and Cancer: A Review of Clinical Implications of Senescence and Senotherapies (2020) · cites this paper as [21]
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References 91 · Cited by 64
- Authors
- Bharadwaj, D., & Mandal, M.
- Affiliations
- Indian Institute of Technology Kharagpur (IN)
- Corresponding author
- Mandal, Mahitosh
- ORCID
- Mandal, Mahitosh
- Venue
- Cytokine & Growth Factor Reviews
- Publisher
- Elsevier BV
- Published
- 2020-04
- Volume
- 52
- Pages
- 68-75
- ISSN
- 1359-6101 (ISSN-L)
- OpenAlex
- W2988065899
- Cited by
- 64
- References
- 91
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 11 · 2023: 8 · 2022: 6 · 2021: 12 · 2020: 11 · 2019: 1
- FWCI
- 0.89
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cytokine & Growth Factor Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Human Resource Development
- Indian Institute of Technology Kharagpur
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- cellular senescence, chemoresistance, tumor microenvironment, senescence-associated secretory phenotype, genotoxic stress, chemotherapy-induced senescence, acquired drug resistance, senolytics
- MeSH terms
- Aging, Animals, Antineoplastic Agents, Cell Transformation, Neoplastic, Humans, Neoplasms, Phenotype, Polyploidy, Signal Transduction, Giant Cells, Cytokines, Cellular Senescence, Drug Resistance, Neoplasm, Intercellular Signaling Peptides and Proteins, Mice, Tumor Microenvironment, Carcinogenesis
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