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Senescence in tumours: evidence from mice and humans
Open accessAbstract
The importance of cellular senescence, which is a stress response that stably blocks proliferation, is increasingly being recognized. Senescence is prevalent in pre-malignant tumours, and progression to malignancy requires evading senescence. Malignant tumours, however, may still undergo senescence owing to interventions that restore tumour suppressor function or inactivate oncogenes. Senescent tumour cells can be cleared by immune cells, which may result in efficient tumour regression. Standard chemotherapy also has the potential to induce senescence, which may partly underlie its therapeutic activity. Although these concepts are well supported in mouse models, translating them to clinical oncology remains a challenge.
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“There is little doubt that the senescence growth arrest suppresses the development of cancer (8, 48, 136).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [136]
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In the citing paper
“Other senescence markers have been shown to be overexpressed or activated in cancer152.”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [152]
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In the citing paper
“Whatever the case, the examples above, and a growing list of similar studies (Collado and Serrano, 2010), argue that cellular senescence restrains cancer by imposing a cell-autonomous block to the proliferation of oncogenically damaged/stressed cells (Fig. 2).”
From Four faces of cellular senescence (2011) · cites this paper as Collado and Serrano, 2010
In the citing paper
“A SASP profile can be further determined by the activation of molecular cascades linked to p53/p21 (due to persistent double strands breaks/telomere shortening)”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [24]
In the citing paper
“but also to p16/Rb (due to epigenetic modifications) [3,22,24,25,26]”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [24]
In the citing paper
“It is believed that senescence is a key mechanism by which p53 suppresses tumorigenesis (Braig and Schmitt, 2006; Collado and Serrano, 2010).”
From p53-dependent chemokine production by senescent tumor cells supports NKG2D-dependent tumor elimination by natural killer cells (2013) · cites this paper as Collado and Serrano, 2010
In the citing paper
“Therefore, it has been proposed that senescence escape is required for tumor progression to overt malignancy [18,21].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [21]
In the citing paper
“However, senescence has also been implicated both in promoting carcinogenesis 15 and in age-related pathologies 16,17 through its autocrine and paracrine effects, known as the senescence-associated secretory phenotype (SASP) originally described by the Campisi group.18,19”
From Senescence from G2 arrest, revisited (2015) · cites this paper as [15]
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BackgroundBAG2 is a target of the c-Myc gene and is involved in cellular senescence via the p21CIP1 pathway
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“Studies in mouse models of oncogenic Ras expression have also shown that pre-malignant lesions contain a relative abundance of senescent cells, suggesting that entry into senescence is one of the mechanisms utilised by cells to prevent full malignant transformation (33).”
BackgroundMiz1 Is a Critical Repressor of cdkn1a during Skin Tumorigenesis
Hönnemann, J., Sanz‐Moreno, A., Wolf, E., Eilers, M., & Elsässer, H. (2012) · PLoS ONE · doi:10.1371/journal.pone.0034885 · Cited by 17
“senescence during tumor formation [44,45].”
Jones, K. A., Gilder, A. S., Lam, M. S., Du, N., Banki, M. A., Merati, A., Pizzo, D. P., VandenBerg, S. R., & Gonias, S. L. (2015) · Neuro-Oncology · doi:10.1093/neuonc/nov243 · Cited by 17
The Potential Role of Senescence As a Modulator of Platelets and Tumorigenesis
Valenzuela, C. A., Quintanilla, R., Moore‐Carrasco, R., & Brown, N. E. (2017) · Frontiers in Oncology · doi:10.3389/fonc.2017.00188 · Cited by 18
Nanocarriers targeting senescent cells
Muñoz‐Espín, D. (2019) · Translational Medicine of Aging · doi:10.1016/j.tma.2019.01.001 · Cited by 17
Dong, H., Hu, L., Li, W., Shi, M., He, L., Wang, C., Hu, Y., Wang, H. H., Wen, C., Liu, H., et al. (2022) · Molecular Biology Reports · doi:10.1007/s11033-022-07262-y · Cited by 17
“Many reports have shown that the p53 signaling pathway is closely related to cellular senescence [14].”
BackgroundMDM2 Overexpression, Activation of Signaling Networks, and Cell Proliferation
Deb, S. P., Singh, S., & Deb, S. (2014) · Sub-cellular biochemistry/Subcellular biochemistry · doi:10.1007/978-94-017-9211-0_12 · Cited by 18
Xiao, Y., Zou, P., Wang, J., Song, H. K., Zou, J., & Liu, L. (2012) · Journal of Huazhong University of Science and Technology [Medical Sciences] · doi:10.1007/s11596-012-0057-z · Cited by 17
Recent Advances in Senolysis for Age-Related Diseases
Aratani, S., & Nakanishi, M. (2023) · Physiology · doi:10.1152/physiol.00003.2023 · Cited by 16
Glutamine addiction and therapeutic strategies in pancreatic cancer
Ren, L., Mao, T., Meng, P., Zhang, L., Wei, H., & Tian, Z. (2023) · World Journal of Gastrointestinal Oncology · doi:10.4251/wjgo.v15.i11.1852 · Cited by 16
“Cancer cell progression is inhibited by cellular senescence, which causes cell cycle arrest in damaged or dysfunctional cells[44].”
Cellular senescence by loss of Men1 in osteoblasts is critical for age‐related osteoporosis
Ukon, Y., Kaito, T., Hirai, H., Kitahara, T., Bun, M., Kodama, J., Tateiwa, D., Nakagawa, S., Ikuta, M., Furuichi, T., et al. (2024) · Aging Cell · doi:10.1111/acel.14254 · Cited by 15
“Senescent cells are identi�ed at high frequencies in benign tumors, whereas they are rarely detected in malignant tumors 39,40 .”
BackgroundMcGowan, E. M., Tran, N., Alling, N., Yagoub, D., Sedger, L. M., & Martiniello‐Wilks, R. (2012) · PLoS ONE · doi:10.1371/journal.pone.0042246 · Cited by 16
“Senescence is regarded as a strong protective response in aging or abnormal cells, whereby cells can enter irreversible mitogenrefractory growth arrest to prevent tumourigenesis [53,54,55,56].”
BackgroundSmall Molecule Inhibitors Targeting Key Proteins in the DNA Damage Response for Cancer Therapy
Li, L., Kumar, A. K., Hu, Z., & Guo, Z. (2020) · Current Medicinal Chemistry · doi:10.2174/0929867327666200224102309 · Cited by 17
Kudlová, N., Slavík, H., Dušková, P., Fürst, T., Srovnal, J., Bártek, J., Mistrík, M., & Hajdúch, M. (2021) · Aging · doi:10.18632/aging.203744 · Cited by 16
Myoepithelial and luminal breast cancer cells exhibit different responses to all-trans retinoic acid
Berardi, D. E., Flumián, C., Campodónico, P. B., Urtreger, A. J., Bessone, M. I. D., Motter, A. N., Joffé, E. B. D. K., Farias, E., & Todaro, L. B. (2015) · Cellular Oncology · doi:10.1007/s13402-015-0230-z · Cited by 16
“It is important to highlight here that many of the senescence related genes do not harbour RARE sites in their promoters [82, 83].”
Succoio, M., Comegna, M., DˈAmbrosio, C., Scaloni, A., Cimino, F., & Faraonio, R. (2015) · Journal of Proteomics · doi:10.1016/j.jprot.2015.07.010 · Cited by 16
“In addition, several endogenous or exogenous stresses including reactive oxygen species (ROS), ionizing/ultraviolet irradiations, and oncogenic insults have been demonstrated to induce prematurely a senescence phenotype [2–4].”
BackgroundLanigan, F. T., Brien, G. L., Fan, Y., Madden, S. F., Jerman, E., Maratha, A., Aloraifi, F., Hokamp, K., Dunne, E. J., Lohan, A. J., et al. (2015) · FEBS Journal · doi:10.1111/febs.13354 · Cited by 17
Leung, E. Y. L., McMahon, J. D., McLellan, D. R., Syyed, N., McCarthy, C., Nixon, C., Orange, C., Brock, C., Hunter, K. D., & Adams, P. D. (2017) · Histopathology · doi:10.1111/his.13260 · Cited by 16
“Hence, improved understanding of the molecular mechanisms underlying the progression from OD to OSCC could help to stratify risks of patients with OD and streamline their follow-up, with the potential to identify malignant transformation early, while minimizing morbidity from active surveillance and repeat resections.…”
BackgroundSenescent tumor cells building three-dimensional tumor clusters
Lee, H.-G., Kim, J. H., Sun, W., Chi, S.-G., Choi, W., & Lee, K. J. (2018) · Scientific Reports · doi:10.1038/s41598-018-28963-0 · Cited by 15
Palazzo, A., Hernández‐Vargas, H., Goehrig, D., Médard, J., Vindrieux, D., Flaman, J., & Bernard, D. (2022) · Cancer Letters · doi:10.1016/j.canlet.2022.215850 · Cited by 15
Selenoproteins and the senescence-associated epitranscriptome
Lee, M. Y., Ojeda-Britez, S., Ehrbar, D. J., Samwer, A., Begley, T. J., & Melendez, J. A. (2022) · Experimental Biology and Medicine · doi:10.1177/15353702221116592 · Cited by 16
Wuestefeld, A., Iakovleva, V., Yap, S. X. L., Ong, A. B. L., Huang, D. Q., Shuen, T. W. H., Toh, H. C., Dan, Y. Y., Zender, L., & Wüestefeld, T. (2022) · Cancer Research · doi:10.1158/0008-5472.can-22-1477 · Cited by 17
Senescence program and its reprogramming in pancreatic premalignancy
Yang, K., Li, X., & Xie, K. (2023) · Cell Death and Disease · doi:10.1038/s41419-023-06040-3 · Cited by 20
“If mutated KARS is expressed in cells with intact cell cycle checkpoints, it can trigger OIS resulting in cell cycle arrest in the G1 phase, thus preventing further tissue transformation [77].”
BackgroundStrategies to make human skin models based on cellular senescence for ageing research
Shakel, Z., Lima, S. A. C., & Reis, S. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102430 · Cited by 17
“Furthermore, the senescence mechanism has significant importance in pre-malignant tumours and restricts the proliferation of cells with irreparable DNA damage (Collado and Serrano, 2010).”
BackgroundLandragin, C., Saichi, M., Laisné, M., Durand, A., Prompsy, P., Leclère, R., Mesple, J., Borgman, K. J. E., Trouchet, A., Faraldo, M. M., et al. (2025) · Molecular Cancer · doi:10.1186/s12943-025-02331-9 · Cited by 13
Ceteci, F., Xu, J., Ceteci, S., Zanucco, E., Thakur, C., & Rapp, U. R. (2011) · Neoplasia · doi:10.1593/neo.11652 · Cited by 16
“Another cell autonomous mechanism that restricts tumor growth is oncogene-induced senescence, an irreversible form of growth arrest [17,23].”
BackgroundReduced Geminin levels promote cellular senescence
Iliou, M. S., Kotantaki, P., Karamitros, D., Σπέλλα, Μ., Taraviras, S. L., & Lygerou, Z. (2012) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2012.10.001 · Cited by 15
Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia
Bellelli, R., Vitagliano, D., Federico, G., Marotta, P., Tamburrino, A., Salerno, P., Paciello, O., Papparella, S., Knauf, J. A., Fagin, J. A., et al. (2017) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2017.06.023 · Cited by 15
“OIS has been 15 demonstrated in human precancerous lesions and it is considered a major barrier against 16 tumorigenesis (Collado and Serrano, 2010; Negrini et al., 2010).”
BackgroundResultFrancica, P., Aebersold, D. M., & Medová, M. (2016) · Biochemical Pharmacology · doi:10.1016/j.bcp.2016.08.022 · Cited by 15
“Even though it is not yet completely clear what determines whether cells undergo cell death or senescence in response to genotoxic insults, both biological processes were shown to be unique or concomitant critical components of the tumor cell response to various anticancer approaches, including RTKs targeting strategi…”
InfluentialTurrini, E., Catanzaro, E., Ferruzzi, L., Guerrini, A., Tacchini, M., Sacchetti, G., Paganetto, G., Maffei, F., Pellicioni, V., Poli, F., et al. (2019) · Scientific Reports · doi:10.1038/s41598-019-43609-5 · Cited by 15
Fatty acid oxidation regulates cellular senescence by modulating the autophagy-SIRT1 axis
Yang, S., Moon, S., Hur, S. C., & Jeong, S. M. (2023) · BMB Reports · doi:10.5483/bmbrep.2023-0076 · Cited by 14
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“Cellular senescence does not necessarily harm tumor growth 27 or wound healing.”
BackgroundSenotherapy, cancer, and aging
Balducci, L., Falandry, C., & Monfardini, S. (2023) · Journal of Geriatric Oncology · doi:10.1016/j.jgo.2023.101671 · Cited by 16
Xiong, J., Fu, Y., Huang, J., Wang, Y., Jin, X., Wan, X., Huang, L., & Huang, Z. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1265525 · Cited by 14
Xu, M., Xia, Z.-Y., Sun, J., Liu, C., An, Y., Xu, J., Zhang, S.-H., Zhong, X., Zeng, N., Ma, S., et al. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1395047 · Cited by 14
“…prevent the dephosphorylation of Phosphatidylinositol-3,4,5-triphosphate (PIP3), leading to the activation of the PI3K/AKT signaling pathway (61, 62). p27kip1, a Cyclin-dependent kinase inhibitor, attaches to CDK2, blocking its kinase activity and halting cell cycle progression. p27 has a high…”
Wang, T., Shi, X., Xu, X., Zhang, J., Ma, Z., Meng, C., Jiao, D., Wang, Y., Chen, Y., He, Z., et al. (2025) · Biomaterials · doi:10.1016/j.biomaterials.2025.123129 · Cited by 14
Upregulation of SOX4 antagonizes cellular senescence in esophageal squamous cell carcinoma
Han, R., Huang, S., Bao, Y., Liu, X. Z., Peng, X., Chen, Z., Wang, Q., Wang, J., Zhang, Q., Wang, T., et al. (2016) · Oncology Letters · doi:10.3892/ol.2016.4799 · Cited by 14
“However, the direct evidence of senescence in cancer tissues is limited (22).”
Peeper, D. S. (2011) · Nature · doi:10.1038/479186a · Cited by 14
Markelic, M., Drača, D., Krajnović, T., Jović, Z., Vuksanović, M., Koruga, D., Mijatović, S., & Maksimović-Ivanić, D. (2022) · Nanomaterials · doi:10.3390/nano12081331 · Cited by 10
Metadata
- Authors
- Collado, M., & Serrano, M.
- Affiliations
- Spanish National Cancer Research Centre (ES)
- Venue
- Nature Reviews Cancer
- Published
- 2010-01
- Volume
- 10
- Issue
- 1
- Pages
- 51-57
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- PMC
- PMC3672965
- OpenAlex
- W2087999409
- Cited by
- 1,124
- References
- 58
- Citations by year
- 2026: 34 · 2025: 40 · 2024: 56 · 2023: 73 · 2022: 60 · 2021: 64 · 2020: 47 · 2019: 67 · 2018: 66 · 2017: 66 · 2016: 73 · 2015: 81 · 2014: 104 · 2013: 102 · 2012: 82
- FWCI
- 6.97
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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
- oncogene-induced senescence, cellular senescence, tumor suppressor function, tumor regression, chemotherapy-induced senescence, senescence therapy, mouse tumor model
- MeSH terms
- Animals, Disease Models, Animal, Humans, Neoplasms, Cellular Senescence, Mice
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