[1] Sun Y, Coppé JP, Lam EWF. Cellular senescence: the sought or the unwanted?. Trends Mol Med, 2018; 24, 871−85. doi:  10.1016/j.molmed.2018.08.002
[2] Sadaie M, Dillon C, Narita M, et al. Cell-based screen for altered nuclear phenotypes reveals senescence progression in polyploid cells after Aurora kinase B inhibition. Mol Biol Cell, 2015; 26, 2971−85. doi:  10.1091/mbc.E15-01-0003
[3] Wang LQ, Lankhorst L, Bernards R. Exploiting senescence for the treatment of cancer. Nat Rev Cancer, 2022; 22, 340−55. doi:  10.1038/s41568-022-00450-9
[4] Coppé JP, Patil CK, Rodier F, et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. PLoS Biol, 2008; 6, e301. doi:  10.1371/journal.pbio.0060301
[5] Eggert T, Wolter K, Ji JL, et al. Distinct functions of senescence-associated immune responses in liver tumor surveillance and tumor progression. Cancer Cell, 2016; 30, 533−47. doi:  10.1016/j.ccell.2016.09.003
[6] Guo YN, Ayers JL, Carter KT, et al. Senescence-associated tissue microenvironment promotes colon cancer formation through the secretory factor GDF15. Aging Cell, 2019; 18, e13013.
[7] Milanovic M, Fan DNY, Belenki D, et al. Senescence-associated reprogramming promotes cancer stemness. Nature, 2018; 553, 96−100. doi:  10.1038/nature25167
[8] Tonnessen-Murray CA, Frey WD, Rao SG, et al. Chemotherapy-induced senescent cancer cells engulf other cells to enhance their survival. J Cell Biol, 2019; 218, 3827−44. doi:  10.1083/jcb.201904051
[9] Sieben CJ, Sturmlechner I, van de Sluis B, et al. Two-step senescence-focused cancer therapies. Trends Cell Biol, 2018; 28, 723−37. doi:  10.1016/j.tcb.2018.04.006
[10] Saleh T, Carpenter VJ, Bloukh S, et al. Targeting tumor cell senescence and polyploidy as potential therapeutic strategies. Semin Cancer Biol, 2022; 81, 37−47. doi:  10.1016/j.semcancer.2020.12.010
[11] Roger L, Tomas F, Gire V. Mechanisms and regulation of cellular senescence. Int J Mol Sci, 2021; 22, 13173. doi:  10.3390/ijms222313173
[12] Mao ZY, Ke ZH, Gorbunova V, et al. Replicatively senescent cells are arrested in G1 and G2 phases. Aging (Albany NY), 2012; 4, 431−5.
[13] Ye CY, Zhang XR, Wan JH, et al. Radiation-induced cellular senescence results from a slippage of long-term G2 arrested cells into G1 phase. Cell Cycle, 2013; 12, 1424−32. doi:  10.4161/cc.24528
[14] Zhang XR, Liu YA, Sun F, et al. p21 is responsible for ionizing radiation-induced bypass of mitosis. Biomed Environ Sci, 2016; 29, 484−93.
[15] Johmura Y, Shimada M, Misaki T, et al. Necessary and sufficient role for a mitosis skip in senescence induction. Mol Cell, 2014; 55, 73−84. doi:  10.1016/j.molcel.2014.05.003
[16] Krenning L, Feringa FM, Shaltiel IA, et al. Transient activation of p53 in G2 phase is sufficient to induce senescence. Mol Cell, 2014; 55, 59−72. doi:  10.1016/j.molcel.2014.05.007
[17] Nam HJ, van Deursen JM. Cyclin B2 and p53 control proper timing of centrosome separation. Nat Cell Biol, 2014; 16, 535−46. doi:  10.1038/ncb2952
[18] Lénárt P, Petronczki M, Steegmaier M, et al. The small-molecule inhibitor BI 2536 reveals novel insights into mitotic roles of polo-like kinase 1. Curr Biol, 2007; 17, 304−15. doi:  10.1016/j.cub.2006.12.046
[19] Kim CH, Kim DE, Kim DH, et al. Mitotic protein kinase-driven crosstalk of machineries for mitosis and metastasis. Exp Mol Med, 2022; 54, 414−25. doi:  10.1038/s12276-022-00750-y
[20] Tavernier N, Sicheri F, Pintard L. Aurora A kinase activation: different means to different ends. J Cell Biol, 2021; 220, e202106128. doi:  10.1083/jcb.202106128
[21] Marumoto T, Honda S, Hara T, et al. Aurora-A kinase maintains the fidelity of early and late mitotic events in HeLa cells. J Biol Chem, 2003; 278, 51786−95. doi:  10.1074/jbc.M306275200
[22] Satinover DL, Brautigan DL, Stukenberg PT. Aurora-A kinase and inhibitor-2 regulate the cyclin threshold for mitotic entry in Xenopus early embryonic cell cycles. Cell Cycle, 2006; 5, 2268−74. doi:  10.4161/cc.5.19.3316
[23] Macůrek L, Lindqvist A, Lim D, et al. Polo-like kinase-1 is activated by aurora A to promote checkpoint recovery. Nature, 2008; 455, 119−23. doi:  10.1038/nature07185
[24] Seki A, Coppinger JA, Jang CY, et al. Bora and the kinase Aurora a cooperatively activate the kinase Plk1 and control mitotic entry. Science, 2008; 320, 1655−8. doi:  10.1126/science.1157425
[25] Hernandez-Segura A, Nehme J, Demaria M. Hallmarks of cellular senescence. Trends Cell Biol, 2018; 28, 436−53. doi:  10.1016/j.tcb.2018.02.001
[26] He JP, Li JH, Ye CY, et al. Cell cycle suspension: a novel process lurking in G2 arrest. Cell Cycle, 2011; 10, 1468−76. doi:  10.4161/cc.10.9.15510
[27] Sakaue-Sawano A, Kurokawa H, Morimura T, et al. Visualizing spatiotemporal dynamics of multicellular cell-cycle progression. Cell, 2008; 132, 487−98. doi:  10.1016/j.cell.2007.12.033
[28] Weigel MT, Dowsett M. Current and emerging biomarkers in breast cancer: prognosis and prediction. Endocr Relat Cancer, 2010; 17, R245−62. doi:  10.1677/ERC-10-0136
[29] Takahashi A, Imai Y, Yamakoshi K, et al. DNA damage signaling triggers degradation of histone methyltransferases through APC/CCdh1 in senescent cells. Mol Cell, 2012; 45, 123−31. doi:  10.1016/j.molcel.2011.10.018
[30] Davan-Wetton CSA, Pessolano E, Perretti M, et al. Senescence under appraisal: hopes and challenges revisited. Cell Mol Life Sci, 2021; 78, 3333−54. doi:  10.1007/s00018-020-03746-x
[31] Bunz F, Dutriaux A, Lengauer C, et al. Requirement for p53 and p21 to sustain G2 arrest after DNA damage. Science, 1998; 282, 1497−501. doi:  10.1126/science.282.5393.1497
[32] Wiebusch L, Hagemeier C. p53- and p21-dependent premature APC/C-Cdh1 activation in G2 is part of the long-term response to genotoxic stress. Oncogene, 2010; 29, 3477−89. doi:  10.1038/onc.2010.99
[33] Schrock MS, Stromberg BR, Scarberry L, et al. APC/C ubiquitin ligase: functions and mechanisms in tumorigenesis. Semin Cancer Biol, 2020; 67, 80−91. doi:  10.1016/j.semcancer.2020.03.001
[34] Goldenson B, Crispino JD. The aurora kinases in cell cycle and leukemia. Oncogene, 2015; 34, 537−45. doi:  10.1038/onc.2014.14
[35] Qi JL, Gao X, Zhong XM, et al. Selective inhibition of Aurora A and B kinases effectively induces cell cycle arrest in t(8;21) acute myeloid leukemia. Biomed Pharmacother, 2019; 117, 109113. doi:  10.1016/j.biopha.2019.109113
[36] Yan M, Wang CL, He B, et al. Aurora-a kinase: a potent oncogene and target for cancer therapy. Med Res Rev, 2016; 36, 1036−79. doi:  10.1002/med.21399
[37] Mou PK, Yang EJ, Shi CX, et al. Aurora kinase A, a synthetic lethal target for precision cancer medicine. Exp Mol Med, 2021; 53, 835−47. doi:  10.1038/s12276-021-00635-6
[38] Zhu Y, Tchkonia T, Pirtskhalava T, et al. The Achilles' heel of senescent cells: from transcriptome to senolytic drugs. Aging Cell, 2015; 14, 644−58. doi:  10.1111/acel.12344
[39] Baker DJ, Childs BG, Durik M, et al. Naturally occurring p16Ink4a-positive cells shorten healthy lifespan. Nature, 2016; 530, 184−9. doi:  10.1038/nature16932
[40] Chang JH, Wang YY, Shao LJ, et al. Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice. Nat Med, 2016; 22, 78−83. doi:  10.1038/nm.4010
[41] Duerr J, Leitz DHW, Szczygiel M, et al. Conditional deletion of Nedd4-2 in lung epithelial cells causes progressive pulmonary fibrosis in adult mice. Nat Commun, 2020; 11, 2012. doi:  10.1038/s41467-020-15743-6
[42] Rangarajan S, Locy ML, Chanda D, et al. Mitochondrial uncoupling protein-2 reprograms metabolism to induce oxidative stress and myofibroblast senescence in age-associated lung fibrosis. Aging Cell, 2022; 21, e13674.
[43] Baar MP, Brandt RMC, Putavet DA, et al. Targeted apoptosis of senescent cells restores tissue homeostasis in response to chemotoxicity and aging. Cell, 2017; 169, 132-47. e16. doi:  10.1016/j.cell.2017.02.031
[44] Borghesan M, Hoogaars WMH, Varela-Eirin M, et al. A senescence-centric view of aging: implications for longevity and disease. Trends Cell Biol, 2020; 30, 777−91. doi:  10.1016/j.tcb.2020.07.002
[45] Kudlova N, De Sanctis JB, Hajduch M. Cellular senescence: molecular targets, biomarkers, and senolytic drugs. Int J Mol Sci, 2022; 23, 4168. doi:  10.3390/ijms23084168