Cellular senescence in cancers: relationship between bone marrow cancer and cellular senescence

Springer Science and Business Media LLC - Tập 49 - Trang 4003-4012 - 2022
Manizheh Sarikhani1, Masoumeh Firouzamandi1
1Biotechnology Section, Department of Pathobiology, Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran

Tóm tắt

There are many factors and conditions that lead to cellular senescence. Replicative senescence and Hayflick phenomenon are the most important causes of cellular senescence. Senescent cells also lead to wound healing conditions resulting from injury and toxic conditions. When a cell becomes senescent, it stops replication and begins to leak inflammatory signals before growth. It also alters the extracellular matrix and behavior of neighbor cells and even motivates them. This review was conducted to determine the association between senescence and bone marrow cancer. The results showed that senescent cells have a short life span due to their self-destructive nature or natural removal from the body by the immune system. These signals are effective to a certain extent in regenerating the damaged cells when present in a transient state. Cellular senescence can decrease the risk of all cancers, including bone marrow cancer, ensuring that cells with significant DNA injury are prevented from replication. However, senescent cells increase in number as they age, which is very harmful over time. These cells extend into an older tissue for longer periods of time and form longer clusters in older tissues. Therefore, cellular senescence significantly contributes to aging.

Tài liệu tham khảo

Hayflick L (1965) The limited in vitro lifetime of human diploid cell strains. Exp Cell Res 37(3):614–636. https://doi.org/10.1016/0014-4827(65)90211-9 Foreman KJ, Marquez N, Dolgert A et al (2018) Forecasting life expectancy, years of life lost, and all-cause and cause-specific mortality for 250 causes of death: reference and alternative scenarios for 2016–40 for 195 countries and territories. Lancet 392(10159):2052–2090. https://doi.org/10.1016/S0140-6736(18)31694-5 Juliusson G, Antunovic P, Derolf A et al (2009) Age and acute myeloid leukemia: real world data on decision to treat and outcomes from the Swedish Acute Leukemia Registry. Blood 113:4179–4187. https://doi.org/10.1182/blood-2008-07-172007 Hellmich C, Moore JA, Bowles KM, Rushworth SA (2020) Bone marrow senescence and the microenvironment of hematological malignancies. Front Oncol 10(3389):2020–00230. https://doi.org/10.3389/fonc.2020.00230 Miraki-Moud F, Anjos-Afonso F, Hodby KA et al (2013) Acute myeloid leukemia does not deplete normal hematopoietic stem cells but induces cytopenias by impeding their differentiation. Proc Natl Acad Sci USA 110(33):13576–13581. https://doi.org/10.1073/pnas.1301891110 Al-Matary YS, Botezatu L, Opalka B et al (2016) Acute myeloid leukemia cells polarize macrophages towards a leukemia supporting state in a growth factor independence one dependent manner. Haematologica 101:1216–1227. https://doi.org/10.3324/haematol.2016.143180 Piddock RE, Bowles KM, Rushworth SA (2017) The role of PI3K isoforms in regulating bone marrow microenvironment signaling focusing on acute myeloid leukemia and multiple myeloma. Cancers 9:29. https://doi.org/10.3390/cancers9040029 Piddock RE, Marlein CR, Abdul-Aziz A et al (2018) Myeloma-derived macrophage inhibitory factor regulates bone marrow stromal cell-derived IL-6 via c-MYC. Int J Hematol Oncol Stem Cell Res 11:66. https://doi.org/10.1186/s13045-018-0614-4 Stanulla M, Schrappe M (2009) Treatment of childhood acute lymphoblastic leukemia. Semin Hematol 46(1):52–63. https://doi.org/10.1053/j.seminhematol.2008.09.007 Pui CH, Relling MV, Downing JR (2004) Acute lymphoblastic leukemia. N Engl J Med 350(15):1535–1548. https://doi.org/10.1056/NEJMra023001 Howard SC, Metzger ML, Wilimas JA, Quintana Y, Pui CH, Robison LL, Ribeiro RC (2008) Childhood cancer epidemiology in low-income countries. Cancer Cancer 112(3):461–472. https://doi.org/10.1002/cncr.23205 Linabery AM, Ross JA (2008) Trends in childhood cancer incidence in the US (1992–2004). Cancer 112(2):416–432. https://doi.org/10.1002/cncr.23169 Redaelli A, Laskin BL, Stephens JM, Botteman MF, Pashos CL (2005) A systematic literature review of the clinical and epidemiological burden of acute lymphoblastic leukaemia (ALL). Eur J Cancer Care 14(1):53–62. https://doi.org/10.1111/j.1365-2354.2005.00513.x Spix C, Eletr D, Blettner M, Kaatsch P (2008) Temporal trends in the incidence rate of childhood cancer in Germany 1987–2004. Int J Cancer 122(8):1859–1867. https://doi.org/10.1002/ijc.23281 Swaminathan R, Rama R, Shanta V (2008) Childhood cancers in Chennai, India, 1990–2001: incidence and survival. Int J Cancer 122(11):2607–2611. https://doi.org/10.1002/ijc.23428 Chen Y, Li J, Zhao Z (2021) Redox control in acute lymphoblastic leukemia: from physiology to pathology and therapeutic opportunities. Cells 10(5):1218. https://doi.org/10.3390/cells10051218 Ehrenfeld V, Fulda S (2020) Thioredoxin inhibitor PX-12 induces mitochondria-mediated apoptosis in acute lymphoblastic leukemia cells. BIOL CHEM 401(2):273–283. https://doi.org/10.1515/hsz-2019-0160 Prieto-Bermejo R, Romo-González M, Pérez-Fernández A, Ijurko C, Hernández-Hernández Á (2018) Reactive oxygen species in haematopoiesis: leukaemic cells take a walk on the wild side. J Exp Clin Cancer Res 37(1):1–18. https://doi.org/10.1186/s13046-018-0797-0 Demaria M, Ohtani N, Youssef SA et al (2014) An essential role for senescent cells in optimal wound healing through secretion of PDGF-AA. Dev Cell 31(6):722–733. https://doi.org/10.1016/j.devcel.2014.11.012 Campisi J (2013) Aging, cellular senescence, and cancer. Annu Rev Physiol 75:685–705. https://doi.org/10.1146/annurev-physiol-030212-183653 Childs BG, Baker DJ, Kirkland JL et al (2014) Senescence and apoptosis: dueling or complementary cell fates. EMBO Rep 15:1139–53. https://doi.org/10.15252/embr.201439245 Yosef R, Pilpel N, Tokarsky-Amiel R et al (2016) Directed elimination of senescent cells by inhibition of BCL-W and BCL-XL. Nat Commun 7:11190. https://doi.org/10.1038/ncomms11190 Bakar DJ, Wijshake T, Tchkonia T et al (2011) Clearance of p16Ink4a-positive senescent cells delays aging-associated disorders. Nature 479:232–236. https://doi.org/10.1038/nature10600 Burd CE, Sorrentino JA, Clark KS et al (2013) Monitoring tumorigenesis and senescence in vivo with a p16(INK4a)-luciferase model. Cell 152:340–351. https://doi.org/10.1016/j.cell.2012.12.010 Patil P, Dong Q, Wang D et al (2019) Systemic clearance of p16INK4a-positive senescent cells mitigates age-associated intervertebral disc degeneration. Aging Cell 18(3):e12927. https://doi.org/10.1111/acel.12927 Hellmich C, Moore JA, Bowles KM et al (2020) Bone marrow senescence and the microenvironment of hematological malignancies. Front Oncol. https://doi.org/10.3389/fonc.2020.00230 Doulatov S, Notta F, Laurenti E et al (2012) Hematopoisiesis: a human perspective. Cell Stem Cell 10:120–136. https://doi.org/10.1016/j.stem.2012.01.006 Geiger H, de Haan G, Florian MC (2013) The ageing haematopoietic stem cell compartment. Nat Rev Immunol 13:376–389. https://doi.org/10.1038/nri3433 Delia D, Mizutani S (2017) The DNA damage response pathway in normal hematopoiesis and malignancies. Int J Hematol 106(3):328–334. https://doi.org/10.1007/s12185-017-2300-7 Chambers SM, Shaw CA, Gatza C et al (2007) Aging hematopoietic stem cells decline in function and exhibit epigenetic dysregulation. PLoS Biol 5(8):e201. https://doi.org/10.1371/journal.pbio.0050201 Beerman I, Maloney WJ, Weissmann IL et al (2010) Stem cells and the aging hematopoitic system. Curr Opin Immunol 22:500–506. https://doi.org/10.1016/j.coi.2010.06.007 Shafat MS, Gnaneswaran B, Bowles KM et al (2017) The bone marrow microenvironment - home of the leukemic blasts. Blood Rev 31:277–286. https://doi.org/10.1016/j.blre.2017.03.004 Sun Y, Campisi J, Higano C et al (2012) Treatment-induced damage to the tumor microenvironment promotes prostate cancer therapy resistance through WNT16B. Nat Med 18(9):1359–1368. https://doi.org/10.1038/nm.2890 Grimwade D, Walker H, Harrison G et al (2001) The predictive value of hierarchical cytogenetic classification in older adults with acute myeloid leukemia (AML): analysis of 1065 patients entered into the United Kingdom Medical Research Council AML11 trial. Blood 98(5):1312–1320. https://doi.org/10.1182/blood.V98.5.1312 Abdul-Aziz AM, Sun Y, Hellmich C et al (2019) Acute myeloid leukemia induces protumoral p16INK4a-driven senescence in the bone marrow microenvironment. Blood 133:446–456. https://doi.org/10.1182/blood-2018-04-845420 André T, Meuleman N, Stamatopoulos B et al (2013) Evidences of early senescence in multiple myeloma bone marrow mesenchymal stromal cells. PLoS ONE 8:e59756. https://doi.org/10.1371/journal.pone.0059756 Guo J, Zhao Y, Fei C et al (2018) Dicer1 downregulation by multiple myeloma cells promotes the senescence and tumor-supporting capacity and decreases the differentiation potential of mesenchymal stem cells. Cell Death Dis 9(5):1–15. https://doi.org/10.1038/s41419-018-0545-6 Deininger MW, Tyner JW, Solary E (2017) Turning the tide in myelodysplastic/myeloproliferative neoplasms. Nat Rev Cancer 17(7):425–440. https://doi.org/10.1038/nrc.2017.40 Sánchez-Aguilera A, Arranz L, Martín-Pérez D, García-García A, Stavropoulou V, Kubovcakova L, Isern J, Martín-Salamanca S, Langa X, Skoda RC, Schwaller J (2014) Estrogen signaling selectively induces apoptosis of hematopoietic progenitors and myeloid neoplasms without harming steady-state hematopoiesis. Cell Stem Cell 15(6):791–804. https://doi.org/10.1016/j.stem.2014.11.002 Ho YH, Méndez-Ferrer S (2020) Microenvironmental contributions to hematopoietic stem cell aging. Haematologica 105(1):38. https://doi.org/10.3324/haematol.2018.211334 Baker DJ, Wijshake T, Tchkonia T et al (2011) Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature 479:232–236. https://doi.org/10.1038/nature10600 Baar MP, Brandt RMC, Putavet DA et al (2017) Targeted apoptosis of senescent cells restores tissue homeostasis in response to chemotoxicity and Senescent. Cell 169:132–47.e16. https://doi.org/10.1016/j.cell.2017.02.031 Demaria M, O’Leary MN, Chang J et al (2017) Cellular senescence promotes adverse effects of chemotherapy and cancer relapse. Cancer Discov 7:165–176. https://doi.org/10.1158/2159-8290.CD-16-0241 Hanahan D, Weinberg RA (2011) Hallmarks of cancer: the next generation. Cell 144(5):646–674. https://doi.org/10.1016/j.cell.2011.02.013 Ewald JA, Desotelle JA, Wilding G et al (2010) Therapy-induced senescence in cancer. J Natl Cancer Inst 102:1536–1546. https://doi.org/10.1093/jnci/djq364 Kamijo T, Zindy F, Roussel MF et al (1997) Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19 ARF. Cell 91(5):649–659. https://doi.org/10.1016/S0092-8674(00)80452-3 Vergel M, Marin JJ, Estevez P et al (2011) Cellular senescence as a target in cancer control. Aging Res. https://doi.org/10.4061/2011/725365 Lodish H, BerK A, Krieger M et al (2008) Title of chapter in sentence style capitalization. In: Hurst M (ed) Molecular cell biology, vol 21, 5th edn. W. H. Freeman, New York, pp 881–890 Rubin H (2009) The disparity between human cell senescence in vitro and lifelong replication in vivo. Nat Biotechnol 20(7):675–681. https://doi.org/10.1038/nbt0702-675 Jaiswal S, Natarajan P, Silver AJ et al (2017) Clonal hematopoiesis and risk of atherosclerotic cardiovascular disease. N Engl J Med 377:111–121. https://doi.org/10.1056/NEJMoa1701719 Cavanaugh A, Juengst B, Sheridan K et al (2015) Combined inhibition of heat shock proteins 90 and 70 leads to simultaneous degradation of the oncogenic signaling proteins involved in muscle invasive bladder cancer. Oncotarget 6(37):39821. https://doi.org/10.18632/oncotarget.5496 Leal J, Ferrer I, Blanco-Aparicio C et al (2008) S-adenosylhomocysteine hydrolase downregulation contributes to tumorigenesis. Carcinogenesis 29(11):2089–2095. https://doi.org/10.1093/carcin/bgn198 McHugh D, Gil J (2018) Senescence and aging: causes, consequences, and therapeutic avenues. Int J Cell Biol 217(1):65–77. https://doi.org/10.1083/jcb.201708092 Van Deursen JM (2014) The role of senescent cells in ageing. Nature 509(7501):439–446. https://doi.org/10.1038/nature13193 Barnes PJ, Baker J, Donnelly LE (2019) Cellular senescence as a mechanism and target in chronic lung diseases. Am J Respir Crit Care Med 200(5):556–564. https://doi.org/10.1164/rccm.201810-1975TR Davalos AR, Coppe JP, Campisi J et al (2010) Senescent cells as a source of inflammatory factors for tumor progression. Cancer Metastasis Rev 29(2):273–283. https://doi.org/10.1007/s10555-010-9220-9 Shay JW, Roninson IB (2004) Hallmarks of senescence in carcinogenesis and cancer therapy. Oncogene 23(16):2919–2933. https://doi.org/10.1038/sj.onc.1207518 Ventura A, Kirsch DG, McLaughlin ME et al (2007) Restoration of p53 function leads to tumour regression in vivo. Nature 445(7128):661–665. https://doi.org/10.1038/nature05541 Xue W, Zender L, Miething C et al (2007) Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas. Nature 445(7128):656–660. https://doi.org/10.1038/nature05529 Döhner H, Estey E, Grimwade D et al (2017) Diagnosis and management of AML in adults: 2017 ELN recommendations from an international expert panel. Blood 129:424–447. https://doi.org/10.1182/blood-2016-08-733196 Sanoff HK, Deal AM, Krishnamurthy J et al (2014) Effect of cytotoxic chemotherapy on markers of molecular age in patients with breast cancer. J Natl Cancer Inst. https://doi.org/10.1093/jnci/dju057 Schmitt CA, Fridman JS, Yang M et al (2002) A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapy. Cell 109(3):335–346. https://doi.org/10.1016/S0092-8674(02)00734-1 Schwarze SR, Fu VX, Desotelle JA et al (2005) The identification of senescence-specific genes during the induction of senescence in prostate cancer cells. Neoplasia 7(9):816–823. https://doi.org/10.1593/neo.05250 Moiseeva O, Mallette FA, Mukhopadhyay UK et al (2006) DNA damage signaling and p53-dependent senescence after prolonged β-interferon stimulation. Mol Biol Cell 17(4):1583–1592. https://doi.org/10.1091/mbc.e05-09-0858 Shafat MS, Gnaneswaran B, Bowles KM et al (2017) The bone marrow microenvironment–Home of the leukemic blasts. Blood Rev 31(5):277–286. https://doi.org/10.1016/j.blre.2017.03.004 Vergel M, Carnero A (2010) Bypassing cellular senescence by genetic screening tools. Clin Transl Oncol 12(6):410–417. https://doi.org/10.1007/s12094-010-0528-2 He JL, Zhang Y, Mei TT et al (2019) Telomerase-triggered DNAzyme spiders for exponential amplified assay of cancer cells. Biosens Bioelectron 144:111692. https://doi.org/10.1016/j.bios.2019.111692 Liu JY, Souroullas GP, Diekman BO et al (2019) Cells exhibiting strong p16INK4a promoter activation in vivo display features of senescence. Proc Natl Acad Sci USA 116(7):2603–2611. https://doi.org/10.1073/pnas.1818313116 Kawano Y, Moschetta M, Manier S et al (2015) Targeting the bone marrow microenvironment in multiple myeloma. Immunol Rev 263:160–172. https://doi.org/10.1007/978-3-319-40320-5_6 Vulliamy TJ, Marrone A, Knight SW et al (2006) Mutations in dyskeratosis congenita: their impact on telomere length and the diversity of clinical presentation. Blood 107(7):2680–2685. https://doi.org/10.1182/blood-2005-07-2622 Artandi SE, DePinho RA (2000) Mice without telomerase: what can they teach us about human cancer? Nat Med 6(8):852–855. https://doi.org/10.1038/78595 Souers AJ, Leverson JD, Boghaert ER et al (2013) ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets. Nat Med 19(2):202–208. https://doi.org/10.1038/nm.3048 Xu M, Pirtskhalava T, Farr JN et al (2018) Senolytics improve physical function and increase lifespan in old age. Nat Med 24:1246–1256. https://doi.org/10.1038/s41591-018-0092-9 Sommer A, Royle NJ (2020) ALT: a multi-faceted phenomenon. Genes 11(2):133. https://doi.org/10.3390/genes11020133 Baker JR, Donnelly LE, Barnes PJ (2020) Senotherapy: a new horizon for COPD therapy. Chest 158(2):562–570. https://doi.org/10.1016/j.chest.2020.01.027 Baker DJ et al (2016) Naturally occurring p16 Ink4a-positive cells shorten healthy lifespan. Nature 530(7589):184–189. https://doi.org/10.1038/nature16932 Wyld L et al (2020) Senescence and cancer: a review of clinical implications of senescence and senotherapies. Cancers 12(8):2134. https://doi.org/10.3390/cancers12082134 Nardella C et al (2011) Pro-senescence therapy for cancer treatment. Nat Rev Cancer 11(7):503–511. https://doi.org/10.1038/nrc3057 Ritschka B et al (2017) The senescence-associated secretory phenotype induces cellular plasticity and tissue regeneration. Genes Dev 31(2):172–183. https://doi.org/10.1101/gad.290635.116 Childs BG et al (2017) Senescent cells: an emerging target for diseases of ageing. Nat Rev Drug Discov 16(10):718–735. https://doi.org/10.1038/nrd.2017.116 Kaefer A et al (2014) Mechanism-based pharmacokinetic/pharmacodynamic meta-analysis of navitoclax (ABT-263) induced thrombocytopenia. Cancer Chemother Pharmacol 74(3):593–602. https://doi.org/10.1007/s00280-014-2530-9 Tse C et al (2008) ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor. Cancer Res 68(9):3421–3428. https://doi.org/10.1158/0008-5472.CAN-07-5836 Dörr JR et al (2013) Synthetic lethal metabolic targeting of cellular senescence in cancer therapy. Nature 501(7467):421–425. https://doi.org/10.1038/nature12437 Kirkland JL, Tchkonia T (2017) Cellular senescence: a translational perspective. EBioMedicine 21:21–28. https://doi.org/10.1016/j.ebiom.2017.04.013 Tchkonia T, Kirkland JL (2018) Aging, cell senescence, and chronic disease: emerging therapeutic strategies. JAMA 320(13):1319–1320. https://doi.org/10.1001/jama.2018.12440 Yousefzadeh MJ et al (2018) Fisetin is a senotherapeutic that extends health and lifespan. EBioMedicine 36:18–28. https://doi.org/10.1016/j.ebiom.2018.09.015