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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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“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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“Indeed, it is necessary for neoplastic cells to bypass the senescence phenotype, typically through loss of p53 and/or Rb, for preneoplasia to progress to frank neoplasia, and on to malignancy (44, 45).”
PIM1 induces cellular senescence through phosphorylation of UHRF1 at Ser311
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“In contrast to reversible cell cycle arrest, cellular senescence is defined by irreversible loss of proliferative potential, acquisition of characteristic morphology, and expression of specific biomarkers, such as SA β-gal (8,17).”
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“The details of how these and other pathways lead to the activation of senescence are now beginning to emerge (d’Adda di Fagagna et al., 2003; Adams, 2009; Collado and Serrano, 2010).”
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“However, stress-inducing stimuli were later shown to activate senescence programmes prior to reaching the cellular replicative limit (premature types), which led to the identification of SIPS [1,3,11].”
BackgroundInfluentialERK pathway agonism for cancer therapy: evidence, insights, and a target discovery framework
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“It is now well accepted that OIS is a key mechanism occurring at the early steps of the tumorigenesis process that prevents the development of malignant tumors from premalignant cells (Braig and Schmitt 2006; Collado and Serrano 2010).”
Circumventing senescence is associated with stem cell properties and metformin sensitivity
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“In addition to apoptosis, cellular senescence has been shown to be an important mechanism for suppressing tumour formation in humans and mice [75,76].”
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MethodTipping the Balance: Cdk2 Enables Myc to Suppress Senescence
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“Moreover, radiation and chemotherapy induce senescence in tumors, indicative that cancer cells possess the latent ability to undergo senescence (13,14).”
BackgroundPotassium Channel KCNA1 Modulates Oncogene-Induced Senescence and Transformation
Lallet-Daher, H., Wiel, C., Gitenay, D., Navaratnam, N., Augert, A., Calvé, B. L., Verbeke, S., Carling, D., Aubert, S., Vindrieux, D., et al. (2013) · Cancer Research · doi:10.1158/0008-5472.can-12-3690 · Cited by 54
“After years of debate about the relevance of this observation, a set of in vivo studies revealed the presence of senescence in premalignant tumors and its absence in malignant tumors (4).”
BackgroundRNA activation: Promise as a new weapon against cancer
Lin, Z., Wang, L., Gan, J., & Zhang, H. (2014) · Cancer Letters · doi:10.1016/j.canlet.2014.09.004 · Cited by 52
MicroRNAs, Long Non-Coding RNAs, and Circular RNAs in the Redox Control of Cell Senescence
Lettieri-Barbato, D., Aquilano, K., Punziano, C., Minopoli, G., & Faraonio, R. (2022) · Antioxidants · doi:10.3390/antiox11030480 · Cited by 51
“mor suppressor mechanism [48], a crucial contributor to embryonic morphogenesis [2,3]”
BackgroundmiR-125b induces cellular senescence in malignant melanoma
Nyholm, A. M., Lerche, C. M., Manfé, V., Biskup, E., Johansen, P., Morling, N., Thomsen, B. M., Glud, M., & Gniadecki, R. (2014) · BMC Dermatology · doi:10.1186/1471-5945-14-8 · Cited by 50
“Interestingly, activation of oncogenes provides a potent senescence signal (oncogene-induced-senescence, OIS) which is considered to be an early protective mechanism against development of cancer [3,5-7].”
Kihara, A., Yoshida, H., Watanabe, R., Takahashi, K., Kato, T., Ino, Y., Kitagawa, M., & Hiraoka, N. (2017) · The American Journal of Surgical Pathology · doi:10.1097/pas.0000000000000856 · Cited by 51
Inhibition of nucleotide synthesis promotes replicative senescence of human mammary epithelial cells
Delfarah, A., Parrish, S., Junge, J. A., Yang, J., Seo, F., Li, S., Mac, J., Wang, P., Fraser, S. E., & Graham, N. A. (2019) · Journal of Biological Chemistry · doi:10.1074/jbc.ra118.005806 · Cited by 50
Wong, J. C. T., Hasan, M. R., Rahman, M., Yu, A. C. Y., Chan, S. K., Schaeffer, D. F., Kennecke, H. F., Lim, H. J., Owen, D. A., & Tai, I. T. (2013) · International Journal of Cancer · doi:10.1002/ijc.28180 · Cited by 49
“This is consistent with recent cancer development models whereby an initiating oncogenic event is thought to establish senescent premalignant states and only with loss of senescence markers do overt malignancies develop.(30,31) That NPM1’s biological effects are mediated by p53 is further reassured by the consistent r…”
BackgroundWhy are epididymal tumours so rare?
Yeung, C., Wang, K., & Cooper, T. G. (2012) · Asian Journal of Andrology · doi:10.1038/aja.2012.20 · Cited by 50
Lin, T.-Y., Cheng, Y.-C., Yang, H.-C., Lin, W.-C., Wang, C.-C., Lai, P.-L., & Shieh, S.-Y. (2011) · Oncogene · doi:10.1038/onc.2011.491 · Cited by 51
“Unexpected cell proliferation often triggers cellular senescence, as is observed after oncogene activation or deletion/inactivation of tumor suppressors (Collado and Serrano, 2010).”
BackgroundCancer cell senescence: a new frontier in drug development
Cairney, C. J., Bilsland, A. E., Evans, T. R. J., Roffey, J., Bennett, D. C., Narita, M., Torrance, C. J., & Keith, W. N. (2012) · Drug Discovery Today · doi:10.1016/j.drudis.2012.01.019 · Cited by 50
Marcoux, S., Lê, O., Langlois-Pelletier, C., Laverdière, C., Hatami, A., Robaey, P., & Beausejour, C. M. (2013) · Radiation Oncology · doi:10.1186/1748-717x-8-252 · Cited by 49
Wang, P., Han, L., Shen, H., Wang, P., Lv, C., Zhao, G., Niu, J., Xue, L., Wang, Q. J., Tong, T., et al. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1310972111 · Cited by 51
“OIS indeed occurs in premalignant human tumors and represents an initial barrier for cancer development in vivo (2).”
BackgroundCheung, C., Singh, R., Kalra, R. S., Kaul, S. C., & Wadhwa, R. (2014) · Journal of Biological Chemistry · doi:10.1074/jbc.m114.547208 · Cited by 48
“To further characterize the COE and CSE cells, we performed immunostaining of HP1 , a senescence marker protein (12).”
MethodJung, S. H., Lee, M., Park, H. A., Lee, H., Kang, D., Hwang, H. J., Park, C., Yu, D., Jung, Y. R., Mi-Na, H. O. N. G., et al. (2018) · Cell Death and Differentiation · doi:10.1038/s41418-018-0114-7 · Cited by 48
Zhou, S., Xu, H., Tang, Q., Xia, H., & Bi, F. (2019) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-19-0413 · Cited by 52
“Targeting the MAPK pathway is thought to be a crucial strategy for colorectal carcinoma (5).”
BackgroundCampisi, J. (2013) · Nature · doi:10.1038/nature12844 · Cited by 48
Despars, G., Carbonneau, C. L., Bardeau, P., Coutu, D. L., & Beausejour, C. M. (2013) · PLoS ONE · doi:10.1371/journal.pone.0073206 · Cited by 49
Caveolae control the anti‐inflammatory phenotype of senescent endothelial cells
Powter, E. E., Coleman, P. R., Tran, M. H., Lay, A. J., Bertolino, P., Parton, R. G., Vadas, M. A., & Gamble, J. R. (2014) · Aging Cell · doi:10.1111/acel.12270 · Cited by 48
“Senescence plays a major role in many pathophysiological processes (Adams, 2009; Rodier & Campisi, 2011), including tumour suppression (Collado & Serrano, 2010), inhibition of liver damage (Krizhanovsky et al., 2008), and it is also linked to the progression of aging and age-related pathologies…”
BackgroundHill, K. S., Erdogan, E., Khoór, A., Walsh, M. P., Leitges, M., Murray, N. R., & Fields, A. P. (2013) · Oncogene · doi:10.1038/onc.2013.147 · Cited by 48
Wu, D., Yu, S., Jia, L., Zou, C., Xu, Z., Xiao, L., Wong, K., Ng, C., & Chan, F. L. (2015) · The Journal of Pathology · doi:10.1002/path.4505 · Cited by 47
“It is well characterized that activation of tumour suppressors p53–p21and p16–pRb-involved pathways plays important roles in the regulation of cellular senescence in cancer cells [2].”
BackgroundLiu, Y., Pan, J., Pan, X., Wu, L., Bian, J., Lin, Z., Xue, M., Su, T., Lai, S., Chen, F., et al. (2019) · Molecular Oncology · doi:10.1002/1878-0261.12577 · Cited by 48
The paradox of senescent-marker positive cancer cells: challenges and opportunities
O’Sullivan, E. A., Wallis, R., Mossa, F., & Bishop, C. L. (2024) · npj Aging · doi:10.1038/s41514-024-00168-y · Cited by 50
“16).”
STAT3 as a new autophagy regulator
Jonchère, B., Bélanger, A., Guette, C., Barré, B., & Coqueret, O. (2013) · JAK-STAT · doi:10.4161/jkst.24353 · Cited by 48
Tièche, C. C., Peng, R., Dorn, P., Froment, L., Schmid, R. A., & Marti, T. M. (2016) · BMC Cancer · doi:10.1186/s12885-016-2117-4 · Cited by 47
“Terminal cell cycle arrest is a classic hallmark of senescence, and has been observed after treatment with chemotherapy (reviewed in [17]).”
BackgroundTaschner‐Mandl, S., Schwarz, M., Blaha, J., Kauer, M. O., Kromp, F., Frank, N., Rifatbegovic, F., Weiss, T., Ladenstein, R. L., HOHENEGGER, M., et al. (2015) · Oncotarget · doi:10.18632/oncotarget.6527 · Cited by 46
“The physiological and pathophysiological role of cellular senescence includes organogenesis during embryonic development [11, 12] and organismal aging [13] as well as removal of damaged cells, as seen upon oncogeneactivation in pre-malignant lesions preventing tumor initiation [14].”
Chen, J., Xu, T., Zhu, D., Wang, J., Huang, C., Lyu, L., Hu, B., Sun, W., & Duan, Y. (2016) · Cell Death and Disease · doi:10.1038/cddis.2016.228 · Cited by 47
“It is widely accepted that cell senescence could serve as an effective strategy for tumor suppression.(29) Recent research has promoted the idea that induction of cellular senescence could also play a vital suppressive role in other non-neoplastic diseases such as liver fibrosis.”
BackgroundWang, H., Han, L., Zhao, G., Shen, H., Wang, P., Sun, Z., Xu, C., Su, Y., Li, G., Tong, T., et al. (2016) · Aging Cell · doi:10.1111/acel.12511 · Cited by 48
“Cellular senescence, including oncogene-induced cellular senescence (OIS), is a stable cell cycle arrest which limits the proliferation of damaged cells and acts as a natural barrier against tumor development in vivo (Collado & Serrano, 2010).”
BackgroundSTAT3-mediated SMAD3 activation underlies Oncostatin M-induced Senescence
Bryson, B. L., Junk, D. J., Cipriano, R., & Jackson, M. W. (2016) · Cell Cycle · doi:10.1080/15384101.2016.1259037 · Cited by 47
Yamane, M., Sato, S., Shimizu, E., Shibata, S., Hayano, M., Yaguchi, T., Kamijuku, H., Ogawa, M., Suzuki, T., Mukai, S., et al. (2020) · The FASEB Journal · doi:10.1096/fj.201900218r · Cited by 47
“15,24,26 To determine whether senescent cells with these characteristics are present in cGVHD LGs, we firstly analyzed the mRNA and protein expression of molecules related to (1) the DDR, (2) senescence, and (3) the SASP in cGVHD LGs.”
BackgroundKMT2C methyltransferase domain regulated INK4A expression suppresses prostate cancer metastasis
Limberger, T., Schlederer, M., Trachtová, K., Alonso, I. G. D. L. F., Yang, J., Högler, S., Sternberg, C., Bystrý, V., Oppelt, J., Tichý, B., et al. (2022) · Molecular Cancer · doi:10.1186/s12943-022-01542-8 · Cited by 49
Al-Wahab, Z. R., Mert, İ., Tebbe, C., Chhina, J., Hijaz, M., Morris, R. T., Ali‐Fehmi, R., Giri, S., Munkarah, A. R., & Rattan, R. (2015) · Oncotarget · doi:10.18632/oncotarget.3434 · Cited by 47
Qu, K., Lin, T., Wang, Z., Liu, S., Chang, H., Xu, X., Meng, F., Zhou, L., Wei, J., Tai, M., et al. (2014) · Frontiers of Medicine · doi:10.1007/s11684-014-0327-1 · Cited by 49
“Clinical and preclinical studies have indicated that many anti-tumor manipulations, including chemotherapeutic drugs and radiation, can induce tumor senescence [13,14].”
BackgroundCheng, X. F., Yao, X., Xu, S., Pan, J., Yu, H., Bao, J., Guan, H., Lu, R., & Zhang, L. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.04.074 · Cited by 47
An Update on the Biology of RAS/RAF Mutations in Colorectal Cancer
Nandan, M. O., & Yang, V. W. (2011) · Current Colorectal Cancer Reports · doi:10.1007/s11888-011-0086-1 · Cited by 50
Pawlikowski, J. S., Adams, P. D., & Nelson, D. M. (2013) · Journal of Cell Science · doi:10.1242/jcs.109728 · Cited by 52
“As discussed above, the bypass or escape of a senescence response in premalignant lesions is required for tumour progression (Bennecke et al., 2010; Braig et al., 2005; Chen et al., 2005; Collado and Serrano, 2010; Dankort et al., 2009; Dhomen et al., 2009).”
BackgroundGonzález-Meljem, J. M., & Martínez-Barberá, J. P. (2021) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-021-03798-7 · Cited by 48
“For this, cellular senescence has been widely regarded as an innately protective mechanism that restricts cancer cell proliferation and tumour growth [32, 33].”
BackgroundMammalian cells acquire epigenetic hallmarks of human cancer during immortalization
Tommasi, S., Zheng, A., Weninger, A., Bates, S. E., Li, X. A., Wu, X., Hollstein, M., & Besaratinia, A. (2013) · Nucleic Acids Research · doi:10.1093/nar/gks1051 · Cited by 45
“This suggests a role for senescent cells in the initiation and progression of tumorigenesis (2,5,6).”
BackgroundInfluentialEffect of Cellular Senescence on the Growth of HER2-Positive Breast Cancers
Fluck, M. F. Z., Morancho, B., Vicario, R., Luque-García, A., Escorihuela, M., Villanueva, J., Rubio, I. T., & Arribas, J. (2015) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/djv020 · Cited by 45
Deubiquitinase USP18 Loss Mislocalizes and Destabilizes KRAS in Lung Cancer
Mustachio, L. M., Lu, Y., Tafe, L. J., Memoli, V. A., Rodriguez‐Canales, J., Mino, B., Villalobos, P. A., Wistuba, I. I., Katayama, H., Hanash, S., et al. (2017) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-16-0369 · Cited by 45
Cellular Senescence, Neurological Function, and Redox State
Maciel-Barón, L. Á., Moreno-Blas, D., Morales-Rosales, S. L., González‐Puertos, V. Y., López‐Díazguerrero, N. E., Torres, C. A., Castro‐Obregón, S., & Königsberg, M. (2017) · Antioxidants and Redox Signaling · doi:10.1089/ars.2017.7112 · Cited by 47
“…senescence occurs both in vitro and in vivo (46) and it has been associated with many biological processes such as aging (21), tumor suppression and promotion (23, 137), chronic inflammation (20), embryonic development (118, 156), and recently with neurodegenerative diseases (NDDs) (11, 13, 35).”
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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