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Cancer and Metastasis Reviews
Published in: Cancer and Metastasis Reviews 2/2010

Open Access 01-06-2010

Senescent cells as a source of inflammatory factors for tumor progression

Authors: Albert R. Davalos, Jean-Philippe Coppe, Judith Campisi, Pierre-Yves Desprez

Published in: Cancer and Metastasis Reviews | Issue 2/2010

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Abstract

Cellular senescence, which is associated with aging, is a process by which cells enter a state of permanent cell cycle arrest, therefore constituting a potent tumor suppressive mechanism. Recent studies show that, despite the beneficial effects of cellular senescence, senescent cells can also exert harmful effects on the tissue microenvironment. The most significant of these effects is the acquisition of a senescent-associated secretory phenotype (SASP), which entails a striking increase in the secretion of pro-inflammatory cytokines. Here, we summarize our knowledge of the SASP and the impact it has on tissue microenvironments and ability to stimulate tumor progression.
Literature
1.
2.
3.
Campisi, J. (2001). Cellular senescence as a tumor-suppressor mechanism. Trends in Cell Biology, 11(11), 27–31.CrossRef
4.
Wright, W. E., & Shay, J. W. (2001). Cellular senescence as a tumor-protection mechanism: The essential role of counting. Current Opinion in Genetics and Development, 11, 98–103.PubMedCrossRef
5.
Ben-Porath, I., & Weinberg, R. A. (2004). When cells get stressed: An integrative view of cellular senescence. Journal of Clinical Investigation, 113, 8–13.PubMed
6.
Collins, C. J., & Sedivy, J. M. (2003). Involvement of the INK4a/Arf gene locus in senescence. Aging Cell, 2, 145–150.PubMedCrossRef
7.
Lowe, S. W., & Sherr, C. J. (2003). Tumor suppression by Ink4a-Arf: Progress and puzzles. Current Opinion in Genetics and Development, 13, 77–83.PubMedCrossRef
8.
Ohtani, N., et al. (2004). The p16INK4a-RB pathway: Molecular link between cellular senescence and tumor suppression. Journal of Medical Investigation, 51, 146–153.PubMedCrossRef
9.
Gil, J., & Peters, G. (2006). Regulation of the INK4b–ARF–INK4a tumour suppressor locus: All for one or one for all. Nature Reviews. Molecular Cell Biology, 7, 667–677.PubMedCrossRef
10.
Braig, M., & Schmitt, C. A. (2006). Oncogene-induced senescence: Putting the brakes on tumor development. Cancer Research, 66, 2881–2884.PubMedCrossRef
11.
Shay, J. W., & Roninson, I. B. (2004). Hallmarks of senescence in carcinogenesis and cancer therapy. Oncogene, 23, 2919–2933.PubMedCrossRef
12.
Ventura, A., et al. (2007). Restoration of p53 function leads to tumour regression in vivo. Nature, 445, 661–665.PubMedCrossRef
13.
Xue, W., et al. (2007). Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas. Nature, 445, 656–660.PubMedCrossRef
14.
Campisi, J. (2005). Senescent cells, tumor suppression and organismal aging: Good citizens, bad neighbors. Cell, 120, 513–522.PubMedCrossRef
15.
Jeyapalan, J. C., et al. (2007). Accumulation of senescent cells in mitotic tissue of aging primates. Mechanisms of Ageing and Development, 128, 36–44.PubMedCrossRef
16.
Castro, P., et al. (2003). Cellular senescence in the pathogenesis of benign prostatic hyperplasia. Prostate, 55, 30–38.PubMedCrossRef
17.
Michaloglou, C., et al. (2005). BRAFE600-associated senescence-like cell cycle arrest of human nevi. Nature, 436, 720–724.PubMedCrossRef
18.
Krtolica, A., et al. (2001). Senescent fibroblasts promote epithelial cell growth and tumorigenesis: A link between cancer and aging. Proceedings of the National Academy of Sciences of the United States of America, 98, 12072–12077.PubMedCrossRef
19.
Liu, D., & Hornsby, P. J. (2007). Senescent human fibroblasts increase the early growth of xenograft tumors via matrix metalloproteinase secretion. Cancer Research, 67, 3117–3126.PubMedCrossRef
20.
Bavik, C., et al. (2006). The gene expression program of prostate fibroblast senescence modulates neoplastic epithelial cell proliferation through paracrine mechanisms. Cancer Research, 66, 794–802.PubMedCrossRef
21.
Parrinello, S., et al. (2005). Stromal–epithelial interactions in aging and cancer: Senescent fibroblasts alter epithelial cell differentiation. Journal of Cell Science, 118(Pt 3), 485–496.PubMedCrossRef
22.
Coppe, J. P., et al. (2008). Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. PLoS Biology, 6(12), 2853–2868.PubMedCrossRef
23.
Coppe, J. P., et al. (2010). A human-like senescence-associated secretory phenotype is conserved in mouse cells dependent on physiological oxygen. PLoS ONE, 5(2), e9188.PubMedCrossRef
24.
Campisi, J., & d'Adda di Fagagna, F. (2007). Cellular senescence: When bad things happen to good cells. Nature Reviews. Molecular Cell Biology, 8, 729–740.PubMedCrossRef
25.
26.
Hayflick, L. (1965). The limited in vitro lifetime of human diploid cell strains. Experimental Cell Research, 37, 614–636.PubMedCrossRef
27.
d'Adda di Fagagna, F., et al. (2003). A DNA damage checkpoint response in telomere-initiated senescence. Nature, 426, 194–198.PubMedCrossRef
28.
Dimri, G. P., et al. (1995). A novel biomarker identifies senescent human cells in culture and in aging skin in vivo. Proceedings of the National Academy of Sciences of the United States of America, 92, 9363–9367.PubMedCrossRef
29.
Ben-Porath, I., & Weinberg, R. A. (2005). The signals and pathways activating cellular senescence. International Journal of Biochemistry and Cell Biology, 37(5), 961–976.PubMedCrossRef
30.
Schmitt, C. A. (2003). Senescence, apoptosis and therapy—Cutting the lifelines of cancer. \Nature Reviews. Cancer, 3(4), 286–295.PubMedCrossRef
31.
Martin, G. M. (2005). Genetic modulation of senescent phenotypes in Homo sapiens. Cell, 120, 523–532.PubMedCrossRef
32.
Chien, K. R., & Karsenty, G. (2005). Longevity and lineages: Toward the integrative biology of degenerative diseases in heart, muscle, and bone. Cell, 120(4), 533–544.PubMedCrossRef
33.
34.
Balaban, R. S., Nemoto, S., & Finkel, T. (2005). Mitochondria, oxidants, and aging. Cell, 120, 483–495.PubMedCrossRef
35.
Collado, M., & Serrano, M. (2006). The power and the promise of oncogene-induced senescence markers. Nature Reviews. Cancer, 6, 472–476.PubMedCrossRef
36.
Hill, R., et al. (2005). Selective evolution of stromal mesenchyme with p53 loss in response to epithelial tumorigenesis. Cell, 123, 1001–1011.PubMedCrossRef
37.
Najjar, S. S., Scuteri, A., & Lakatta, E. G. (2005). Arterial aging: Is it an immutable cardiovascular risk factor? Hypertension, 46(3), 454–462.PubMedCrossRef
38.
Kunieda, T., et al. (2006). Angiotensin II induces premature senescence of vascular smooth muscle cells and accelerates the development of atherosclerosis via a p21-dependent pathway. Circulation, 114(9), 953–960.PubMedCrossRef
39.
Krishnamurthy, J., et al. (2004). Ink4a/Arf expression is a biomarker of aging. Journal of Clinical Investigation, 114, 1299–1307.PubMed
40.
Herbig, U., et al. (2004). Telomere shortening triggers senescence of human cells through a pathway involving ATM, p53, and p21(CIP1), but not p16(INK4a). Molecular Cell, 14(4), 501–513.PubMedCrossRef
41.
Narita, M., et al. (2003). Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence. Cell, 113, 703–716.PubMedCrossRef
42.
Collado, M., & Serrano, M. (2010). Senescence in tumours: Evidence from mice and humans. Nature Reviews. Cancer, 10(1), 51–57.PubMedCrossRef
43.
Coppe, J. P., et al. (2010). The senescence-associated secretory phenotype: The dark side of tumor suppression. Annual Review of Pathology: Mechanisms of Disease, 5, 99–118.CrossRef
44.
Coppe, J. P., et al. (2006). Secretion of vascular endothelial growth factor by primary human fibroblasts at senescence. Journal of Biological Chemistry, 281(40), 29568–29574.PubMedCrossRef
45.
Lu, S. Y., et al. (2006). Ripe areca nut extract induces G1 phase arrests and senescence-associated phenotypes in normal human oral keratinocyte. Carcinogenesis, 27(6), 1273–1284.PubMedCrossRef
46.
Sarkar, D., et al. (2004). Human polynucleotide phosphorylase (hPNPaseold-35): A potential link between aging and inflammation. Cancer Research, 64(20), 7473–7478.PubMedCrossRef
47.
Kuilman, T., et al. (2008). Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. Cell, 133, 1019–1031.PubMedCrossRef
48.
Garfinkel, S., et al. (1994). Post-transcriptional regulation of interleukin 1 alpha in various strains of young and senescent human umbilical vein endothelial cells. Proceedings of the National Academy of Sciences of the United States of America, 91(4), 1559–1563.PubMedCrossRef
49.
McLachlan, J. A., et al. (1995). Immunological functions of aged human monocytes. Pathobiology, 63(3), 148–159.PubMedCrossRef
50.
Maier, J. A. M., et al. (1990). Extension of the life-span of human endothelial cells by an interleukin-1a antisense oligomer. Science, 249, 1570–1574.PubMedCrossRef
51.
Kumar, S., Millis, A. J., & Baglioni, C. (1992). Expression of interleukin 1-inducible genes and production of interleukin 1 by aging human fibroblasts. Proceedings of the National Academy of Sciences of the United States America, 89(10), 4683–4687.CrossRef
52.
Palmieri, D., Watson, J. M., & Rinehart, C. A. (1999). Age-related expression of PEDF/EPC-1 in human endometrial stromal fibroblasts: Implications for interactive senescence. Experimental Cell Research, 247(1), 142–147.PubMedCrossRef
53.
Chang, B. D., et al. (2002). Molecular determinants of terminal growth arrest induced in tumor cells by a chemotherapeutic agent. Proceedings of the National Academy of Sciences of the United States of America, 99, 389–394.PubMedCrossRef
54.
Bode-Boger, S. M., Scalera, F., & Martens-Lobenhoffer, J. (2005). Asymmetric dimethylarginine (ADMA) accelerates cell senescence. Vascular Medicine, 10(Suppl 1), S65–S71.PubMedCrossRef
55.
Wang, S., et al. (1996). Characterization of IGFBP-3, PAI-1 and SPARC mRNA expression in senescent fibroblasts. Mechanisms of Ageing and Development, 92(2–3), 121–132.PubMedCrossRef
56.
Grillari, J., et al. (2000). Subtractive hybridization of mRNA from early passage and senescent endothelial cells. Experimental Gerontology, 35(2), 187–197.PubMedCrossRef
57.
Lopez-Bermejo, A., et al. (2000). Characterization of insulin-like growth factor-binding protein-related proteins (IGFBP-rPs) 1, 2, and 3 in human prostate epithelial cells: Potential roles for IGFBP-rP1 and 2 in senescence of the prostatic epithelium. Endocrinology, 141(11), 4072–4080.PubMedCrossRef
58.
Kim, K. H., et al. (2004). Expression of connective tissue growth factor, a biomarker in senescence of human diploid fibroblasts, is up-regulated by a transforming growth factor-beta-mediated signaling pathway. Biochemical and Biophysical Research Communications, 318(4), 819–825.PubMedCrossRef
59.
West, M. D., Pereira-Smith, O. M., & Smith, J. R. (1989). Replicative senescence of human skin fibroblasts correlates with a loss of regulation and overexpression of collagenase activity. Experimental Cell Research, 184, 138–147.PubMedCrossRef
60.
Millis, A. J. T., et al. (1992). Differential expression of metalloproteinase and tissue inhibitor of metalloproteinase genes in diploid human fibroblasts. Experimental Cell Research, 201, 373–379.PubMedCrossRef
61.
Zeng, G., & Millis, A. J. (1996). Differential regulation of collagenase and stromelysin mRNA in late passage cultures of human fibroblasts. Experimental Cell Research, 222(1), 150–156.PubMedCrossRef
62.
Hornebeck, W., & Maquart, F. X. (2003). Proteolyzed matrix as a template for the regulation of tumor progression. Biomedicine and Pharmacotherapy, 57(5–6), 223–230.CrossRef
63.
McQuibban, G. A., et al. (2002). Matrix metalloproteinase processing of monocyte chemoattractant proteins generates CC chemokine receptor antagonists with anti-inflammatory properties in vivo. Blood, 100(4), 1160–1167.PubMed
64.
Blasi, F., & Carmeliet, P. (2002). uPAR: A versatile signalling orchestrator. Nature Reviews. Molecular Cell Biology, 3(12), 932–943.PubMedCrossRef
65.
Sato, I., et al. (1993). Reduction of nitric oxide producing activity associated with in vitro aging in cultured human umbilical vein endothelial cell. Biochemical and Biophysical Research Communications, 195(2), 1070–1076.PubMedCrossRef
66.
Lee, A. C., et al. (1999). Ras proteins induce senescence by altering the intracellular levels of reactive oxygen species. Journal of Biological Chemistry, 274(12), 7936–7940.PubMedCrossRef
67.
van der Loo, B., et al. (2000). Enhanced peroxynitrite formation is associated with vascular aging. Journal of Experimental Medicine, 192(12), 1731–1744.PubMedCrossRef
68.
Macip, S., et al. (2002). Inhibition of p21-mediated ROS accumulation can rescue p21-induced senescence. EMBO Journal, 21, 2180–2188.PubMedCrossRef
69.
Xin, M. G., et al. (2003). Senescence-enhanced oxidative stress is associated with deficiency of mitochondrial cytochrome c oxidase in vascular endothelial cells. Mechanisms of Ageing and Development, 124(8–9), 911–919.PubMedCrossRef
70.
Finkel, T., & Holbrook, N. J. (2000). Oxidants, oxidative stress and the biology of ageing. Nature, 408, 239–247.PubMedCrossRef
71.
Finkel, T., Serrano, M., & Blasco, M. A. (2007). The common biology of cancer and ageing. Nature, 448, 767–774.PubMedCrossRef
72.
Funayama, R., & Ishikawa, F. (2007). Cellular senescence and chromatin structure. Chromosoma, 116(5), 431–440.PubMedCrossRef
73.
Mehta, I. S., et al. (2007). Alterations to nuclear architecture and genome behavior in senescent cells. Annals of the New York Academy of Sciences, 1100, 250–263.PubMedCrossRef
74.
Narita, M. (2007). Cellular senescence and chromatin organisation. British Journal of Cancer, 96(5), 686–691.PubMedCrossRef
75.
76.
Acosta, J. C., et al. (2008). Chemokine signaling via the CXCR2 receptor reinforces senescence. Cell, 133(6), 1006–1018.PubMedCrossRef
77.
Rodier, F., et al. (2009). Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion. Nature Cell Biology, 11(8), 973–979.PubMedCrossRef
78.
d'Adda di Fagagna, F. (2008). Living on a break: Cellular senescence as a DNA-damage response. Nature Reviews. Cancer, 8(7), 512–22.PubMedCrossRef
79.
Hiscott, J., et al. (1993). Characterization of a functional NF-kappa B site in the human interleukin 1 beta promoter: Evidence for a positive autoregulatory loop. Molecular and Cellular Biology, 13(10), 6231–6240.PubMed
80.
Niu, J., et al. (2004). Identification of an autoregulatory feedback pathway involving interleukin-1alpha in induction of constitutive NF-kappaB activation in pancreatic cancer cells. Journal of Biological Chemistry, 279(16), 16452–16462.PubMedCrossRef
81.
Orjalo, A. V., et al. (2009). Cell surface-bound IL-1alpha is an upstream regulator of the senescence-associated IL-6/IL-8 cytokine network. Proceedings of the National Academy of Sciences of the United States of America, 106(40), 17031–17036.PubMedCrossRef
82.
Bhaumik, D., et al. (2009). MicroRNAs miR-146a/b negatively modulate the senescence-associated inflammatory mediators IL-6 and IL-8. Aging, 1(4), 402–411.PubMed
83.
Taganov, K. D., et al. (2006). NF-kappaB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses. Proceedings of the National Academy of Sciences of the United States of America, 103(33), 12481–12486.PubMedCrossRef
84.
Adams, P. D. (2007). Remodeling of chromatin structure in senescent cells and its potential impact on tumor suppression and aging. Gene, 397(1–2), 84–93.PubMedCrossRef
85.
Bianchi, M. E., & Agresti, A. (2005). HMG proteins: Dynamic players in gene regulation and differentiation. Current Opinion in Genetics and Development, 15(5), 496–506.PubMedCrossRef
86.
Lotze, M. T., & Tracey, K. J. (2005). High-mobility group box 1 protein (HMGB1): Nuclear weapon in the immune arsenal. Nature Reviews. Immunology, 5(4), 331–342.PubMedCrossRef
87.
Park, J. S., et al. (2003). Activation of gene expression in human neutrophils by high mobility group box 1 protein. American Journal of Physiology Cell Physiology, 284(4), C870–C879.PubMed
88.
Stros, M., et al. (2004). High-affinity binding of tumor-suppressor protein p53 and HMGB1 to hemicatenated DNA loops. Biochemistry, 43(22), 7215–7225.PubMedCrossRef
89.
Jayaraman, L., et al. (1998). High mobility group protein-1 (HMG-1) is a unique activator of p53. Genes and Development, 12(4), 462–472.PubMedCrossRef
90.
Scaffidi, P., Misteli, T., & Bianchi, M. E. (2002). Release of chromatin protein HMGB1 by necrotic cells triggers inflammation. Nature, 418(6894), 191–195.PubMedCrossRef
91.
Kokkola, R., et al. (2005). RAGE is the major receptor for the proinflammatory activity of HMGB1 in rodent macrophages. Scandinavian Journal of Immunology, 61(1), 1–9.PubMedCrossRef
92.
Rouhiainen, A., et al. (2007). Pivotal advance: Analysis of proinflammatory activity of highly purified eukaryotic recombinant HMGB1 (amphoterin). Journal of Leukocyte Biology, 81(1), 49–58.PubMedCrossRef
93.
Bianchi, M.E., (2009). HMGB1 loves company. J Leukoc Biol.
94.
Sha, Y., et al. (2008). HMGB1 develops enhanced proinflammatory activity by binding to cytokines. Journal of Immunology, 180(4), 2531–2537.
95.
Kokkola, R., et al. (2003). Successful treatment of collagen-induced arthritis in mice and rats by targeting extracellular high mobility group box chromosomal protein 1 activity. Arthritis and Rheumatism, 48(7), 2052–2058.PubMedCrossRef
96.
Elliott, M. R., et al. (2009). Nucleotides released by apoptotic cells act as a find-me signal to promote phagocytic clearance. Nature, 461(7261), 282–286.PubMedCrossRef
97.
Krizhanovsky, V., et al. (2008). Senescence of activated stellate cells limits liver fibrosis. Cell, 134(4), 657–667.PubMedCrossRef
98.
Fages, C., et al. (2000). Regulation of cell migration by amphoterin. Journal of Cell Science, 113(Pt 4), 611–620.PubMed
99.
Schlueter, C., et al. (2005). Angiogenetic signaling through hypoxia: HMGB1: An angiogenetic switch molecule. American Journal of Pathology, 166(4), 1259–1263.PubMed
100.
Taguchi, A., et al. (2000). Blockade of RAGE-amphoterin signalling suppresses tumour growth and metastases. Nature, 405(6784), 354–360.PubMedCrossRef
101.
Brennan, F. M., Maini, R. N., & Feldmann, M. (1995). Cytokine expression in chronic inflammatory disease. British Medical Bulletin, 51(2), 368–384.PubMed
102.
Brod, S. A. (2000). Unregulated inflammation shortens human functional longevity. Inflammation Research, 49(11), 561–570.PubMedCrossRef
103.
Caruso, C., et al. (2004). Aging, longevity, inflammation, and cancer. Annals of the New York Academy of Sciences, 1028, 1–13.PubMedCrossRef
104.
Tsai, K. K., et al. (2005). Cellular mechanisms for low-dose ionizing radiation-induced perturbation of the breast tissue microenvironment. Cancer Research, 65, 6734–6744.PubMedCrossRef
105.
Sun, P., et al. (2007). PRAK is essential for ras-induced senescence and tumor suppression. Cell, 128, 295–308.PubMedCrossRef
106.
Choi, J., et al. (2000). Expression of senescence-associated beta-galactosidase in enlarged prostates from men with benign prostatic hyperplasia. Urology, 56, 160–166.PubMedCrossRef
107.
Ohuchida, K., et al. (2004). Radiation to stromal fibroblasts increases invasiveness of pancreatic cancer cells through tumor–stromal interactions. Cancer Research, 64(9), 3215–3222.PubMedCrossRef
108.
Coppe, J. P., et al. (2008). A role for fibroblasts in mediating the effects of tobacco-induced epithelial cell growth and invasion. Molecular Cancer Research, 6(7), 1085–1098.PubMedCrossRef
109.
Barcellos-Hoff, M. H., & Ravani, S. A. (2000). Irradiated mammary gland stroma promotes the expression of tumorigenic potential by unirradiated epithelial cells. Cancer Research, 60, 1254–1260.PubMed
110.
Yang, F., et al. (2005). Stromal expression of connective tissue growth factor promotes angiogenesis and prostate cancer tumorigenesis. Cancer Research, 65(19), 8887–8895.PubMedCrossRef
111.
Lehmann, B. D., et al. (2008). Senescence-associated exosome release from human prostate cancer cells. Cancer Research, 68, 7864–7871.PubMedCrossRef
112.
Dilley, T. K., Bowden, G. T., & Chen, Q. M. (2003). Novel mechanisms of sublethal oxidant toxicity: Induction of premature senescence in human fibroblasts confers tumor promoter activity. Experimental Cell Research, 290, 38–48.PubMedCrossRef
113.
Dhawan, P., & Richmond, A. (2002). Role of CXCL1 in tumorigenesis of melanoma. Journal of Leukocyte Biology, 72(1), 9–18.PubMed
114.
Balentien, E., et al. (1991). Effects of MGSA/GRO alpha on melanocyte transformation. Oncogene, 6(7), 1115–1124.PubMed
115.
Schadendorf, D., et al. (1993). IL-8 produced by human malignant melanoma cells in vitro is an essential autocrine growth factor. Journal of Immunology, 151(5), 2667–2675.
116.
Bernardini, G., et al. (2000). I-309 binds to and activates endothelial cell functions and acts as an angiogenic molecule in vivo. Blood, 96(13), 4039–4045.PubMed
117.
Salcedo, R., et al. (2001). Eotaxin (CCL11) induces in vivo angiogenic responses by human CCR3+ endothelial cells. Journal of Immunology, 166(12), 7571–7578.
118.
119.
Sparmann, A., & Bar-Sagi, D. (2004). Ras-induced interleukin-8 expression plays a critical role in tumor growth and angiogenesis. Cancer Cell, 6(5), 447–458.PubMedCrossRef
120.
Frey, A. B. (2006). Myeloid suppressor cells regulate the adaptive immune response to cancer. Journal of Clinical Investigation, 116(10), 2587–2590.PubMedCrossRef
121.
Birchmeier, C., et al. (2003). Met, metastasis, motility and more. Nature Reviews. Molecular Cell Biology, 4(12), 915–925.PubMedCrossRef
122.
Camphausen, K., et al. (2001). Radiation therapy to a primary tumor accelerates metastatic growth in mice. Cancer Research, 61(5), 2207–2211.PubMed
123.
Qian, L. W., et al. (2002). Radiation-induced increase in invasive potential of human pancreatic cancer cells and its blockade by a matrix metalloproteinase inhibitor, CGS27023. Clinical Cancer Research, 8(4), 1223–1227.PubMed
124.
Strieter, R. M., et al. (2006). Cancer CXC chemokine networks and tumour angiogenesis. European Journal of Cancer, 42(6), 768–778.PubMedCrossRef
125.
Orr, F. W., & Wang, H. H. (2001). Tumor cell interactions with the microvasculature: A rate-limiting step in metastasis. Surgical Oncology Clinics of North America, 10(2), 357–81. ix−x.PubMed
126.
Nickoloff, B. J., et al. (2004). Tumor suppressor maspin is up-regulated during keratinocyte senescence, exerting a paracrine antiangiogenic activity. Cancer Research, 64(9), 2956–2961.PubMedCrossRef
127.
Mantovani, A. (2004). Chemokines in neoplastic progression. Seminars in Cancer Biology, 14(3), 147–148.PubMedCrossRef
128.
Homey, B., Muller, A., & Zlotnik, A. (2002). Chemokines: Agents for the immunotherapy of cancer? Nature Reviews. Immunology, 2(3), 175–184.PubMedCrossRef
129.
130.
Ben-Baruch, A. (2006). Inflammation-associated immune suppression in cancer: The roles played by cytokines, chemokines and additional mediators. Seminars in Cancer Biology, 16(1), 38–52.PubMedCrossRef
131.
Potempa, S., & Ridley, A. J. (1998). Activation of both MAP kinase and phosphatidylinositide 3-kinase by Ras is required for hepatocyte growth factor/scatter factor-induced adherens junction disassembly. Molecular Biology of the Cell, 9(8), 2185–2200.PubMed
132.
Paumelle, R., et al. (2002). Hepatocyte growth factor/scatter factor activates the ETS1 transcription factor by a RAS–RAF–MEK–ERK signaling pathway. Oncogene, 21(15), 2309–2319.PubMedCrossRef
133.
Thiery, J. P. (2002). Epithelial–mesenchymal transitions in tumour progression. Nature Reviews. Cancer, 2(6), 442–454.PubMedCrossRef
134.
Tonini, T., Rossi, F., & Claudio, P. P. (2003). Molecular basis of angiogenesis and cancer. Oncogene, 22(42), 6549–6556.PubMedCrossRef
135.
Nesbit, M., et al. (2001). Low-level monocyte chemoattractant protein-1 stimulation of monocytes leads to tumor formation in nontumorigenic melanoma cells. Journal of Immunology, 166(11), 6483–6490.
136.
Schaider, H., et al. (2003). Differential response of primary and metastatic melanomas to neutrophils attracted by IL-8. International Journal of Cancer, 103(3), 335–343.CrossRef
137.
Sica, A., et al. (2006). Tumour-associated macrophages are a distinct M2 polarised population promoting tumour progression: Potential targets of anti-cancer therapy. European Journal of Cancer, 42(6), 717–727.PubMedCrossRef
138.
Selivanova, G., et al. (1997). Restoration of the growth suppression function of mutant p53 by a synthetic peptide derived from the p53 C-terminal domain. Nature Medicine, 3(6), 632–638.PubMedCrossRef
139.
Foster, B. A., et al. (1999). Pharmacological rescue of mutant p53 conformation and function. Science, 286(5449), 2507–2510.PubMedCrossRef
140.
Chene, P. (2003). Inhibiting the p53–MDM2 interaction: An important target for cancer therapy. Nature Reviews. Cancer, 3(2), 102–109.PubMedCrossRef
141.
Selivanova, G., & Wiman, K. G. (2007). Reactivation of mutant p53: Molecular mechanisms and therapeutic potential. Oncogene, 26(15), 2243–2254.PubMedCrossRef
142.
Barnes, P. J., & Karin, M. (1997). Nuclear factor-kappaB: A pivotal transcription factor in chronic inflammatory diseases. New England Journal of Medicine, 336(15), 1066–1071.PubMedCrossRef
Metadata
Title
Senescent cells as a source of inflammatory factors for tumor progression
Authors
Albert R. Davalos
Jean-Philippe Coppe
Judith Campisi
Pierre-Yves Desprez
Publication date
01-06-2010
Publisher
Springer US
Published in
Cancer and Metastasis Reviews / Issue 2/2010
Print ISSN: 0167-7659
Electronic ISSN: 1573-7233
DOI
https://doi.org/10.1007/s10555-010-9220-9

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