摘要
最近，化学治疗药物诱导的细胞衰老被认为是一种很有前景的抗癌方法。 药物诱导的衰老表现出来自复制和癌基因诱导的衰老的相似和不同的标志，被认为是体外和体内肿瘤对化疗反应的关键决定因素。 迄今为止，已经报道了一定量的能够引起癌细胞衰老的有效化学治疗药物。 这些药物的靶标存在显着差异，包括衰老信号传导途径，DNA复制过程，DNA损伤途径，表观遗传修饰，微管聚合，衰老相关分泌表型（SASP）等。 通过总结诱导衰老的小分子药物及其特定的性状和相应的机制，本综述致力于通过诱导衰老开发新的抗癌治疗策略。
关键词: 癌症，衰老，小分子药物，DNA损伤反应，衰老相关的信号通路，SASP
图形摘要
[1]
Hayflick, L. The limited in vitro lifetime of human diploid cell strains. Exp. Cell Res., 1965, 37, 614-636.
[2]
Hayflick, L.; Moorhead, P.S. The serial cultivation of human diploid cell strains. Exp. Cell Res., 1961, 25, 585-621.
[3]
Chang, B.D.; Broude, E.V.; Dokmanovic, M.; Zhu, H.; Ruth, A.; Xuan, Y.; Kandel, E.S.; Lausch, E.; Christov, K.; Roninson, I.B. A senescence-like phenotype distinguishes tumor cells that undergo terminal proliferation arrest after exposure to anticancer agents. Cancer Res., 1999, 59(15), 3761-3767.
[4]
te Poele, R.H.; Okorokov, A.L.; Jardine, L.; Cummings, J.; Joel, S.P. DNA damage is able to induce senescence in tumor cells in vitro and in vivo. Cancer Res., 2002, 62(4), 1876-1883.
[5]
Roberson, R.S.; Kussick, S.J.; Vallieres, E.; Chen, S.Y.; Wu, D.Y. Escape from therapy-induced accelerated cellular senescence in p53-null lung cancer cells and in human lung cancers. Cancer Res., 2005, 65(7), 2795-2803.
[6]
Schmitt, C.A.; Fridman, J.S.; Yang, M.; Lee, S.; Baranov, E.; Hoffman, R.M.; Lowe, S.W. A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapy. Cell, 2002, 109(3), 335-346.
[7]
Prieur, A.; Besnard, E.; Babled, A.; Lemaitre, J.M. p53 and p16(INK4A) independent induction of senescence by chromatin-dependent alteration of S-phase progression. Nat. Commun., 2011, 2, 473.
[8]
Tu, Z.; Aird, K.M.; Zhang, R. Chromatin remodeling, BRCA1, SAHF and cellular senescence. Cell Cycle, 2013, 12(11), 1653-1654.
[9]
Tu, Z.; Zhuang, X.; Yao, Y.G.; Zhang, R. BRG1 is required for formation of senescence-associated heterochromatin foci induced by oncogenic RAS or BRCA1 loss. Mol. Cell. Biol., 2013, 33(9), 1819-1829.
[10]
Krtolica, A.; Parrinello, S.; Lockett, S.; Desprez, P.Y.; Campisi, J. Senescent fibroblasts promote epithelial cell growth and tumorigenesis: a link between cancer and aging. Proc. Natl. Acad. Sci. USA, 2001, 98(21), 12072-12077.
[11]
Parrinello, S.; Coppe, J.P.; Krtolica, A.; Campisi, J. Stromal-epithelial interactions in aging and cancer: senescent fibroblasts alter epithelial cell differentiation. J. Cell Sci., 2005, 118(Pt 3), 485-496.
[12]
Zhang, Y.; Gao, Y.; Zhao, L.; Han, L.; Lu, Y.; Hou, P.; Shi, X.; Liu, X.; Tian, B.; Wang, X.; Huang, B.; Lu, J. Mitogen-activated protein kinase p38 and retinoblastoma protein signalling is required for DNA damage-mediated formation of senescence-associated heterochromatic foci in tumour cells. FEBS J., 2013, 280(18), 4625-4639.
[13]
Campisi, J. Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. Cell, 2005, 120(4), 513-522.
[14]
Coppe, J.P.; Desprez, P.Y.; Krtolica, A.; Campisi, J. The senescence-associated secretory phenotype: the dark side of tumor suppression. Annu. Rev. Pathol., 2010, 5, 99-118.
[15]
Bavik, C.; Coleman, I.; Dean, J.P.; Knudsen, B.; Plymate, S.; Nelson, P.S. The gene expression program of prostate fibroblast senescence modulates neoplastic epithelial cell proliferation through paracrine mechanisms. Cancer Res., 2006, 66(2), 794-802.
[16]
Frey, A.B. Myeloid suppressor cells regulate the adaptive immune response to cancer. J. Clin. Invest., 2006, 116(10), 2587-2590.
[17]
Chen, P.; Guo, H.; Chen, J.; Fu, Y. The chemotherapeutic drug boanmycin induces cell senescence and senescence-associated secretory phenotype factors, thus acquiring the potential to remodel the tumor microenvironment. Anticancer Drugs, 2016, 27(2), 84-88.
[18]
Bringold, F.; Serrano, M. Tumor suppressors and oncogenes in cellular senescence. Exp. Gerontol., 2000, 35(3), 317-329.
[19]
Lundberg, A.S.; Hahn, W.C.; Gupta, P.; Weinberg, R.A. Genes involved in senescence and immortalization. Curr. Opin. Cell Biol., 2000, 12(6), 705-709.
[20]
Dimauro, T.; David, G. Ras-induced senescence and its physiological relevance in cancer. Curr. Cancer Drug Targets, 2010, 10(8), 869-876.
[21]
Karnoub, A.E.; Weinberg, R.A. Ras oncogenes: split personalities. Nat. Rev. Mol. Cell Biol., 2008, 9(7), 517-531.
[22]
Tu, Z.; Aird, K.M.; Bitler, B.G.; Nicodemus, J.P.; Beeharry, N.; Xia, B.; Yen, T.J.; Zhang, R. Oncogenic RAS regulates BRIP1 expression to induce dissociation of BRCA1 from chromatin, inhibit DNA repair, and promote senescence. Dev. Cell, 2011, 21(6), 1077-1091.
[23]
Tu, Z.; Aird, K.M.; Zhang, R. RAS, cellular senescence and transformation: the BRCA1 DNA repair pathway at the crossroads. Small GTPases, 2012, 3(3), 163-167.
[24]
Jacobs, J.J.; Keblusek, P.; Robanus-Maandag, E.; Kristel, P.; Lingbeek, M.; Nederlof, P.M.; van Welsem, T.; van de Vijver, M.J.; Koh, E.Y.; Daley, G.Q.; van Lohuizen, M. Senescence bypass screen identifies TBX2, which represses Cdkn2a (p19(ARF)) and is amplified in a subset of human breast cancers. Nat. Genet., 2000, 26(3), 291-299.
[25]
Astle, M.V.; Hannan, K.M.; Ng, P.Y.; Lee, R.S.; George, A.J.; Hsu, A.K.; Haupt, Y.; Hannan, R.D.; Pearson, R.B. AKT induces senescence in human cells via mTORC1 and p53 in the absence of DNA damage: implications for targeting mTOR during malignancy. Oncogene, 2012, 31(15), 1949-1962.
[26]
Pearson, M.; Carbone, R.; Sebastiani, C.; Cioce, M.; Fagioli, M.; Saito, S.; Higashimoto, Y.; Appella, E.; Minucci, S.; Pandolfi, P.P.; Pelicci, P.G. PML regulates p53 acetylation and premature senescence induced by oncogenic Ras. Nature, 2000, 406(6792), 207-210.
[27]
Ferbeyre, G.; de Stanchina, E.; Querido, E.; Baptiste, N.; Prives, C.; Lowe, S.W. PML is induced by oncogenic ras and promotes premature senescence. Genes Dev., 2000, 14(16), 2015-2027.
[28]
Boucher, M.J.; Jean, D.; Vezina, A.; Rivard, N. Dual role of MEK/ERK signaling in senescence and transformation of intestinal epithelial cells. Am. J. Physiol. Gastrointest. Liver Physiol., 2004, 286(5), G736-G746.
[29]
Rayess, H.; Wang, M.B.; Srivatsan, E.S. Cellular senescence and tumor suppressor gene p16. Int. J. Cancer, 2012, 130(8), 1715-1725.
[30]
Cordisco, S.; Maurelli, R.; Bondanza, S.; Stefanini, M.; Zambruno, G.; Guerra, L.; Dellambra, E. Bmi-1 reduction plays a key role in physiological and premature aging of primary human keratinocytes. J. Invest. Dermatol., 2010, 130(4), 1048-1062.
[31]
Sagata, N.; Watanabe, N.; Vande Woude, G.F.; Ikawa, Y. The c-mos proto-oncogene product is a cytostatic factor responsible for meiotic arrest in vertebrate eggs. Nature, 1989, 342(6249), 512-518.
[32]
Shibuya, E.K.; Ruderman, J.V. Mos induces the in vitro activation of mitogen-activated protein kinases in lysates of frog oocytes and mammalian somatic cells. Mol. Biol. Cell, 1993, 4(8), 781-790.
[33]
Lin, A.W.; Barradas, M.; Stone, J.C.; van Aelst, L.; Serrano, M.; Lowe, S.W. Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling. Genes Dev., 1998, 12(19), 3008-3019.
[34]
Bartkova, J.; Rezaei, N.; Liontos, M.; Karakaidos, P.; Kletsas, D.; Issaeva, N.; Vassiliou, L.V.; Kolettas, E.; Niforou, K.; Zoumpourlis, V.C.; Takaoka, M.; Nakagawa, H.; Tort, F.; Fugger, K.; Johansson, F.; Sehested, M.; Andersen, C.L.; Dyrskjot, L.; Orntoft, T.; Lukas, J.; Kittas, C.; Helleday, T.; Halazonetis, T.D.; Bartek, J.; Gorgoulis, V.G. Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints. Nature, 2006, 444(7119), 633-637.
[35]
Fujita, N.; Sato, S.; Katayama, K.; Tsuruo, T. Akt-dependent phosphorylation of p27Kip1 promotes binding to 14-3-3 and cytoplasmic localization. J. Biol. Chem., 2002, 277(32), 28706-28713.
[36]
Chu, E.C.; Tarnawski, A.S. PTEN regulatory functions in tumor suppression and cell biology. Med. Sci. Monit., 2004, 10(10), RA235-RA241.
[37]
Mallette, F.A.; Gaumont-Leclerc, M.F.; Ferbeyre, G. The DNA damage signaling pathway is a critical mediator of oncogene-induced senescence. Genes Dev., 2007, 21(1), 43-48.
[38]
Basham, B.; Sathe, M.; Grein, J.; McClanahan, T.; D’Andrea, A.; Lees, E.; Rascle, A. In vivo identification of novel STAT5 target genes. Nucleic Acids Res., 2008, 36(11), 3802-3818.
[39]
Mallette, F.A.; Moiseeva, O.; Calabrese, V.; Mao, B.; Gaumont-Leclerc, M.F.; Ferbeyre, G. Transcriptome analysis and tumor suppressor requirements of STAT5-induced senescence. Ann. N. Y. Acad. Sci., 2010, 1197, 142-151.
[40]
Calabrese, V.; Mallette, F.A.; Deschenes-Simard, X.; Ramanathan, S.; Gagnon, J.; Moores, A.; Ilangumaran, S.; Ferbeyre, G. SOCS1 links cytokine signaling to p53 and senescence. Mol. Cell, 2009, 36(5), 754-767.
[41]
Ferbeyre, G.; Moriggl, R. The role of Stat5 transcription factors as tumor suppressors or oncogenes. Biochim. Biophys. Acta, 2011, 1815(1), 104-114.
[42]
Basu, D.; Reyes-Mugica, M.; Rebbaa, A. Role of the beta catenin destruction complex in mediating chemotherapy-induced senescence-associated secretory phenotype. PLoS One, 2012, 7(12), e52188.
[43]
Yu, S.; Wang, X.; Geng, P.; Tang, X.; Xiang, L.; Lu, X.; Li, J.; Ruan, Z.; Chen, J.; Xie, G.; Wang, Z.; Ou, J.; Peng, Y.; Luo, X.; Zhang, X.; Dong, Y.; Pang, X.; Miao, H.; Chen, H.; Liang, H. Melatonin regulates PARP1 to control the senescence-associated secretory phenotype (SASP) in human fetal lung fibroblast cells. J. Pineal Res., 2017, 63(1)
[44]
Moiseeva, O.; Deschenes-Simard, X.; St-Germain, E.; Igelmann, S.; Huot, G.; Cadar, A.E.; Bourdeau, V.; Pollak, M.N.; Ferbeyre, G. Metformin inhibits the senescence-associated secretory phenotype by interfering with IKK/NF-kappaB activation. Aging Cell, 2013, 12(3), 489-498.
[45]
Macia, A.; Vaquero, M.; Gou-Fabregas, M.; Castelblanco, E.; Valdivielso, J.M.; Anerillas, C.; Mauricio, D.; Matias-Guiu, X.; Ribera, J.; Encinas, M. Sprouty1 induces a senescence-associated secretory phenotype by regulating NFkappaB activity: implications for tumorigenesis. Cell Death Differ., 2014, 21(2), 333-343.
[46]
Coppe, J.P.; Patil, C.K.; Rodier, F.; Sun, Y.; Munoz, D.P.; Goldstein, J.; Nelson, P.S.; Desprez, P.Y.; Campisi, J. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. PLoS Biol., 2008, 6(12), 2853-2868.
[47]
Rodier, F.; Coppe, J.P.; Patil, C.K.; Hoeijmakers, W.A.; Munoz, D.P.; Raza, S.R.; Freund, A.; Campeau, E.; Davalos, A.R.; Campisi, J. Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion. Nat. Cell Biol., 2009, 11(8), 973-979.
[48]
Mantovani, A.; Locati, M.; Vecchi, A.; Sozzani, S.; Allavena, P. Decoy receptors: a strategy to regulate inflammatory cytokines and chemokines. Trends Immunol., 2001, 22(6), 328-336.
[49]
Wajapeyee, N.; Serra, R.W.; Zhu, X.; Mahalingam, M.; Green, M.R. Oncogenic BRAF induces senescence and apoptosis through pathways mediated by the secreted protein IGFBP7. Cell, 2008, 132(3), 363-374.
[50]
Huang, M.; Whang, P.; Lewicki, P.; Mitchell, B.S. Cyclopentenyl cytosine induces senescence in breast cancer cells through the nucleolar stress response and activation of p53. Mol. Pharmacol., 2011, 80(1), 40-48.
[51]
Manfe, V.; Biskup, E.; Johansen, P.; Kamstrup, M.R.; Krejsgaard, T.F.; Morling, N.; Wulf, H.C.; Gniadecki, R. MDM2 inhibitor nutlin-3a induces apoptosis and senescence in cutaneous T-cell lymphoma: role of p53. J. Invest. Dermatol., 2012, 132(5), 1487-1496.
[52]
Ling, X.; Xu, C.; Fan, C.; Zhong, K.; Li, F.; Wang, X. FL118 induces p53-dependent senescence in colorectal cancer cells by promoting degradation of MdmX. Cancer Res., 2014, 74(24), 7487-7497.
[53]
Drosten, M.; Dhawahir, A.; Sum, E.Y.; Urosevic, J.; Lechuga, C.G.; Esteban, L.M.; Castellano, E.; Guerra, C.; Santos, E.; Barbacid, M. Genetic analysis of Ras signalling pathways in cell proliferation, migration and survival. EMBO J., 2010, 29(6), 1091-1104.
[54]
Miliani de Marval, P.L.; Macias, E.; Conti, C.J.; Rodriguez-Puebla, M.L. Enhanced malignant tumorigenesis in Cdk4 transgenic mice. Oncogene, 2004, 23(10), 1863-1873.
[55]
Leontieva, O.V.; Blagosklonny, M.V. CDK4/6-inhibiting drug substitutes for p21 and p16 in senescence: duration of cell cycle arrest and MTOR activity determine geroconversion. Cell Cycle, 2013, 12(18), 3063-3069.
[56]
Leontieva, O.V.; Demidenko, Z.N.; Blagosklonny, M.V. MEK drives cyclin D1 hyperelevation during geroconversion. Cell Death Differ., 2013, 20(9), 1241-1249.
[57]
Perez, M.; Munoz-Galvan, S.; Jimenez-Garcia, M.P.; Marin, J.J.; Carnero, A. Efficacy of CDK4 inhibition against sarcomas depends on their levels of CDK4 and p16ink4 mRNA. Oncotarget, 2015, 6(38), 40557-40574.
[58]
Hu, W.; Sung, T.; Jessen, B.A.; Thibault, S.; Finkelstein, M.B.; Khan, N.K.; Sacaan, A.I. Mechanistic investigation of bone marrow suppression associated with palbociclib and its differentiation from cytotoxic chemotherapies. Clin. Cancer Res., 2016, 22(8), 2000-2008.
[59]
Yoshida, A.; Lee, E.K.; Diehl, J.A. Induction of therapeutic senescence in vemurafenib-resistant melanoma by extended inhibition of CDK4/6. Cancer Res., 2016, 76(10), 2990-3002.
[60]
Rader, J.; Russell, M.R.; Hart, L.S.; Nakazawa, M.S.; Belcastro, L.T.; Martinez, D.; Li, Y.; Carpenter, E.L.; Attiyeh, E.F.; Diskin, S.J.; Kim, S.; Parasuraman, S.; Caponigro, G.; Schnepp, R.W.; Wood, A.C.; Pawel, B.; Cole, K.A.; Maris, J.M. Dual CDK4/CDK6 inhibition induces cell-cycle arrest and senescence in neuroblastoma. Clin. Cancer Res., 2013, 19(22), 6173-6182.
[61]
Park, J.Y.; Park, S.H.; Weiss, R.H. Disparate effects of roscovitine on renal tubular epithelial cell apoptosis and senescence: implications for autosomal dominant polycystic kidney disease. Am. J. Nephrol., 2009, 29(6), 509-515.
[62]
Oliva, J.L.; Caino, M.C.; Senderowicz, A.M.; Kazanietz, M.G. S-Phase-specific activation of PKC alpha induces senescence in non-small cell lung cancer cells. J. Biol. Chem., 2008, 283(9), 5466-5476.
[63]
Mason, S.A.; Cozzi, S.J.; Pierce, C.J.; Pavey, S.J.; Parsons, P.G.; Boyle, G.M. The induction of senescence-like growth arrest by protein kinase C-activating diterpene esters in solid tumor cells. Invest. New Drugs, 2010, 28(5), 575-586.
[64]
Cozzi, S.J.; Parsons, P.G.; Ogbourne, S.M.; Pedley, J.; Boyle, G.M. Induction of senescence in diterpene ester-treated melanoma cells via protein kinase C-dependent hyperactivation of the mitogen-activated protein kinase pathway. Cancer Res., 2006, 66(20), 10083-10091.
[65]
Marusyk, A.; Wheeler, L.J.; Mathews, C.K.; DeGregori, J. p53 mediates senescence-like arrest induced by chronic replicational stress. Mol. Cell. Biol., 2007, 27(15), 5336-5351.
[66]
Maya-Mendoza, A.; Merchut-Maya, J.M.; Bartkova, J.; Bartek, J.; Streuli, C.H.; Jackson, D.A. Immortalised breast epithelia survive prolonged DNA replication stress and return to cycle from a senescent-like state. Cell Death Dis., 2014, 5, e1351.
[67]
Michishita, E.; Nakabayashi, K.; Suzuki, T.; Kaul, S.C.; Ogino, H.; Fujii, M.; Mitsui, Y.; Ayusawa, D. 5-Bromodeoxyuridine induces senescence-like phenomena in mammalian cells regardless of cell type or species. J. Biochem., 1999, 126(6), 1052-1059.
[68]
Suzuki, T.; Minagawa, S.; Michishita, E.; Ogino, H.; Fujii, M.; Mitsui, Y.; Ayusawa, D. Induction of senescence-associated genes by 5-bromodeoxyuridine in HeLa cells. Exp. Gerontol., 2001, 36(3), 465-474.
[69]
Masterson, J.C.; O’Dea, S. 5-Bromo-2-deoxyuridine activates DNA damage signalling responses and induces a senescence-like phenotype in p16-null lung cancer cells. Anticancer Drugs, 2007, 18(9), 1053-1068.
[70]
Nair, R.R.; Bagheri, M.; Saini, D.K. Temporally distinct roles of ATM and ROS in genotoxic-stress-dependent induction and maintenance of cellular senescence. J. Cell Sci., 2015, 128(2), 342-353.
[71]
Yeo, E.J.; Hwang, Y.C.; Kang, C.M.; Kim, I.H.; Kim, D.I.; Parka, J.S.; Choy, H.E.; Park, W.Y.; Park, S.C. Senescence-like changes induced by hydroxyurea in human diploid fibroblasts. Exp. Gerontol., 2000, 35(5), 553-571.
[72]
Hong, S.H.; Hong, B.; Kim, D.C.; Rho, M.S.; Park, J.I.; Rha, S.H.; Jun, H.S.; Jeong, J.S. Involvement of mitogen-activated protein kinases and p21Waf1 in hydroxyurea-induced G1 arrest and senescence of McA-RH7777 rat hepatoma cell line. Exp. Mol. Med., 2004, 36(5), 493-498.
[73]
Park, J.I.; Jeong, J.S.; Han, J.Y.; Kim, D.I.; Gao, Y.H.; Park, S.C.; Rodgers, G.P.; Kim, I.H. Hydroxyurea induces a senescence-like change of K562 human erythroleukemia cell. J. Cancer Res. Clin. Oncol., 2000, 126(8), 455-460.
[74]
Modrak, D.E.; Leon, E.; Goldenberg, D.M.; Gold, D.V. Ceramide regulates gemcitabine-induced senescence and apoptosis in human pancreatic cancer cell lines. Mol. Cancer Res., 2009, 7(6), 890-896.
[75]
Sumikawa, E.; Matsumoto, Y.; Sakemura, R.; Fujii, M.; Ayusawa, D. Prolonged unbalanced growth induces cellular senescence markers linked with mechano transduction in normal and tumor cells. Biochem. Biophys. Res. Commun., 2005, 335(2), 558-565.
[76]
Kobayashi, Y.; Lee, S.S.; Arai, R.; Miki, K.; Fujii, M.; Ayusawa, D. ERK1/2 mediates unbalanced growth leading to senescence induced by excess thymidine in human cells. Biochem. Biophys. Res. Commun., 2012, 425(4), 897-901.
[77]
Robles, S.J.; Adami, G.R. Agents that cause DNA double strand breaks lead to p16INK4a enrichment and the premature senescence of normal fibroblasts. Oncogene, 1998, 16(9), 1113-1123.
[78]
Minieri, V.; Saviozzi, S.; Gambarotta, G.; Lo Iacono, M.; Accomasso, L.; Cibrario Rocchietti, E.; Gallina, C.; Turinetto, V.; Giachino, C. Persistent DNA damage-induced premature senescence alters the functional features of human bone marrow mesenchymal stem cells. J. Cell. Mol. Med., 2015, 19(4), 734-743.
[79]
Mansilla, S.; Pina, B.; Portugal, J. Daunorubicin-induced variations in gene transcription: commitment to proliferation arrest, senescence and apoptosis. Biochem. J., 2003, 372(Pt 3), 703-711.
[80]
Chang, B.D.; Xuan, Y.; Broude, E.V.; Zhu, H.; Schott, B.; Fang, J.; Roninson, I.B. Role of p53 and p21waf1/cip1 in senescence-like terminal proliferation arrest induced in human tumor cells by chemotherapeutic drugs. Oncogene, 1999, 18(34), 4808-4818.
[81]
Elmore, L.W.; Rehder, C.W.; Di, X.; McChesney, P.A.; Jackson-Cook, C.K.; Gewirtz, D.A.; Holt, S.E. Adriamycin-induced senescence in breast tumor cells involves functional p53 and telomere dysfunction. J. Biol. Chem., 2002, 277(38), 35509-35515.
[82]
Sliwinska, M.A.; Mosieniak, G.; Wolanin, K.; Babik, A.; Piwocka, K.; Magalska, A.; Szczepanowska, J.; Fronk, J.; Sikora, E. Induction of senescence with doxorubicin leads to increased genomic instability of HCT116 cells. Mech. Ageing Dev., 2009, 130(1-2), 24-32.
[83]
Spallarossa, P.; Altieri, P.; Aloi, C.; Garibaldi, S.; Barisione, C.; Ghigliotti, G.; Fugazza, G.; Barsotti, A.; Brunelli, C. Doxorubicin induces senescence or apoptosis in rat neonatal cardiomyocytes by regulating the expression levels of the telomere binding factors 1 and 2. Am. J. Physiol. Heart Circ. Physiol., 2009, 297(6), H2169-H2181.
[84]
Leontieva, O.V.; Gudkov, A.V.; Blagosklonny, M.V. Weak p53 permits senescence during cell cycle arrest. Cell Cycle, 2010, 9(21), 4323-4327.
[85]
Litwiniec, A.; Grzanka, A.; Helmin-Basa, A.; Gackowska, L.; Grzanka, D. Features of senescence and cell death induced by doxorubicin in A549 cells: organization and level of selected cytoskeletal proteins. J. Cancer Res. Clin. Oncol., 2010, 136(5), 717-736.
[86]
Jackson, J.G.; Pant, V.; Li, Q.; Chang, L.L.; Quintas-Cardama, A.; Garza, D.; Tavana, O.; Yang, P.; Manshouri, T.; Li, Y.; El-Naggar, A.K.; Lozano, G. p53-mediated senescence impairs the apoptotic response to chemotherapy and clinical outcome in breast cancer. Cancer Cell, 2012, 21(6), 793-806.
[87]
Piegari, E.; De Angelis, A.; Cappetta, D.; Russo, R.; Esposito, G.; Costantino, S.; Graiani, G.; Frati, C.; Prezioso, L.; Berrino, L.; Urbanek, K.; Quaini, F.; Rossi, F. Doxorubicin induces senescence and impairs function of human cardiac progenitor cells. Basic Res. Cardiol., 2013, 108(2), 334.
[88]
Park, C.; Lee, I.; Kang, W.K. E2F-1 is a critical modulator of cellular senescence in human cancer. Int. J. Mol. Med., 2006, 17(5), 715-720.
[89]
Zhao, H.; Halicka, H.D.; Traganos, F.; Jorgensen, E.; Darzynkiewicz, Z. New biomarkers probing depth of cell senescence assessed by laser scanning cytometry. Cytometry A, 2010, 77(11), 999-1007.
[90]
Probin, V.; Wang, Y.; Bai, A.; Zhou, D. Busulfan selectively induces cellular senescence but not apoptosis in WI38 fibroblasts via a p53-independent but extracellular signal-regulated kinase-p38 mitogen-activated protein kinase-dependent mechanism. J. Pharmacol. Exp. Ther., 2006, 319(2), 551-560.
[91]
Litwiniec, A.; Gackowska, L.; Helmin-Basa, A.; Zuryn, A.; Grzanka, A. Low-dose etoposide-treatment induces endoreplication and cell death accompanied by cytoskeletal alterations in A549 cells: Does the response involve senescence? The possible role of vimentin. Cancer Cell Int., 2013, 13(1), 9.
[92]
Velichko, A.K.; Petrova, N.V.; Razin, S.V.; Kantidze, O.L. Mechanism of heat stress-induced cellular senescence elucidates the exclusive vulnerability of early S-phase cells to mild genotoxic stress. Nucleic Acids Res., 2015, 43(13), 6309-6320.
[93]
Wang, X.; Wong, S.C.; Pan, J.; Tsao, S.W.; Fung, K.H.; Kwong, D.L.; Sham, J.S.; Nicholls, J.M. Evidence of cisplatin-induced senescent-like growth arrest in nasopharyngeal carcinoma cells. Cancer Res., 1998, 58(22), 5019-5022.
[94]
Berndtsson, M.; Hagg, M.; Panaretakis, T.; Havelka, A.M.; Shoshan, M.C.; Linder, S. Acute apoptosis by cisplatin requires induction of reactive oxygen species but is not associated with damage to nuclear DNA. Int. J. Cancer, 2007, 120(1), 175-180.
[95]
Qu, K.; Lin, T.; Wang, Z.; Liu, S.; Chang, H.; Xu, X.; Meng, F.; Zhou, L.; Wei, J.; Tai, M.; Dong, Y.; Liu, C. Reactive oxygen species generation is essential for cisplatin-induced accelerated senescence in hepatocellular carcinoma. Front. Med., 2014, 8(2), 227-235.
[96]
Veena, M.S.; Wilken, R.; Zheng, J.Y.; Gholkar, A.; Venkatesan, N.; Vira, D.; Ahmed, S.; Basak, S.K.; Dalgard, C.L.; Ravichandran, S.; Batra, R.K.; Kasahara, N.; Elashoff, D.; Fishbein, M.C.; Whitelegge, J.P.; Torres, J.Z.; Wang, M.B.; Srivatsan, E.S. p16 Protein and gigaxonin are associated with the ubiquitination of NFkappaB in cisplatin-induced senescence of cancer cells. J. Biol. Chem., 2014, 289(50), 34921-34937.
[97]
McKenna, E.; Traganos, F.; Zhao, H.; Darzynkiewicz, Z. Persistent DNA damage caused by low levels of mitomycin C induces irreversible cell senescence. Cell Cycle, 2012, 11(16), 3132-3140.
[98]
Palaniyappan, A. Cyclophosphamide induces premature senescence in normal human fibroblasts by activating MAP kinases. Biogerontology, 2009, 10(6), 677-682.
[99]
Ewald, J.A.; Peters, N.; Desotelle, J.A.; Hoffmann, F.M.; Jarrard, D.F. A high-throughput method to identify novel senescence-inducing compounds. J. Biomol. Screen., 2009, 14(7), 853-858.
[100]
Hirose, Y.; Berger, M.S.; Pieper, R.O. p53 effects both the duration of G2/M arrest and the fate of temozolomide-treated human glioblastoma cells. Cancer Res., 2001, 61(5), 1957-1963.
[101]
Mhaidat, N.M.; Zhang, X.D.; Allen, J.; Avery-Kiejda, K.A.; Scott, R.J.; Hersey, P. Temozolomide induces senescence but not apoptosis in human melanoma cells. Br. J. Cancer, 2007, 97(9), 1225-1233.
[102]
Chen, Q.; Ames, B.N. Senescence-like growth arrest induced by hydrogen peroxide in human diploid fibroblast F65 cells. Proc. Natl. Acad. Sci. USA, 1994, 91(10), 4130-4134.
[103]
Chen, Q.M.; Bartholomew, J.C.; Campisi, J.; Acosta, M.; Reagan, J.D.; Ames, B.N. Molecular analysis of H2O2-induced senescent-like growth arrest in normal human fibroblasts: p53 and Rb control G1 arrest but not cell replication. Biochem. J., 1998, 332(Pt 1), 43-50.
[104]
Frippiat, C.; Dewelle, J.; Remacle, J.; Toussaint, O. Signal transduction in H2O2-induced senescence-like phenotype in human diploid fibroblasts. Free Radic. Biol. Med., 2002, 33(10), 1334-1346.
[105]
Yoshizaki, K.; Fujiki, T.; Tsunematsu, T.; Yamashita, M.; Udono, M.; Shirahata, S.; Katakura, Y. Pro-senescent effect of hydrogen peroxide on cancer cells and its possible application to tumor suppression. Biosci. Biotechnol. Biochem., 2009, 73(2), 311-315.
[106]
Ido, Y.; Duranton, A.; Lan, F.; Cacicedo, J.M.; Chen, T.C.; Breton, L.; Ruderman, N.B. Acute activation of AMP-activated protein kinase prevents H2O2-induced premature senescence in primary human keratinocytes. PLoS One, 2012, 7(4), e35092.
[107]
Suzuki, E.; Takahashi, M.; Oba, S.; Nishimatsu, H. Oncogene- and oxidative stress-induced cellular senescence shows distinct expression patterns of proinflammatory cytokines in vascular endothelial cells. Sci. World J., 2013, 2013, 754735.
[108]
Burova, E.; Borodkina, A.; Shatrova, A.; Nikolsky, N. Sublethal oxidative stress induces the premature senescence of human mesenchymal stem cells derived from endometrium. Oxid. Med. Cell. Longev., 2013, 2013, 474931.
[109]
Borodkina, A.; Shatrova, A.; Abushik, P.; Nikolsky, N.; Burova, E. Interaction between ROS dependent DNA damage, mitochondria and p38 MAPK underlies senescence of human adult stem cells. Aging (Albany N.Y.), 2014, 6(6), 481-495.
[110]
Gorbunova, V.; Seluanov, A.; Pereira-Smith, O.M. Expression of human telomerase (hTERT) does not prevent stress-induced senescence in normal human fibroblasts but protects the cells from stress-induced apoptosis and necrosis. J. Biol. Chem., 2002, 277(41), 38540-38549.
[111]
Chretien, A.; Piront, N.; Delaive, E.; Demazy, C.; Ninane, N.; Toussaint, O. Increased abundance of cytoplasmic and nuclear caveolin 1 in human diploid fibroblasts in H(2)O(2)-induced premature senescence and interplay with p38alpha(MAPK). FEBS Lett., 2008, 582(12), 1685-1692.
[112]
Zdanov, S.; Debacq-Chainiaux, F.; Remacle, J.; Toussaint, O. Identification of p38MAPK-dependent genes with changed transcript abundance in H2O2-induced premature senescence of IMR-90 hTERT human fibroblasts. FEBS Lett., 2006, 580(27), 6455-6463.
[113]
Ota, H.; Eto, M.; Kano, M.R.; Ogawa, S.; Iijima, K.; Akishita, M.; Ouchi, Y. Cilostazol inhibits oxidative stress-induced premature senescence via upregulation of Sirt1 in human endothelial cells. Arterioscler. Thromb. Vasc. Biol., 2008, 28(9), 1634-1639.
[114]
von Zglinicki, T.; Pilger, R.; Sitte, N. Accumulation of single-strand breaks is the major cause of telomere shortening in human fibroblasts. Free Radic. Biol. Med., 2000, 28(1), 64-74.
[115]
Felipe, K.B.; Benites, J.; Glorieux, C.; Sid, B.; Valenzuela, M.; Kviecinski, M.R.; Pedrosa, R.C.; Valderrama, J.A.; Leveque, P.; Gallez, B.; Verrax, J.; Buc Calderon, P. Antiproliferative effects of phenylaminonaphthoquinones are increased by ascorbate and associated with the appearance of a senescent phenotype in human bladder cancer cells. Biochem. Biophys. Res. Commun., 2013, 433(4), 573-578.
[116]
Aoshiba, K.; Tsuji, T.; Nagai, A. Bleomycin induces cellular senescence in alveolar epithelial cells. Eur. Respir. J., 2003, 22(3), 436-443.
[117]
Linge, A.; Weinhold, K.; Blasche, R.; Kasper, M.; Barth, K. Downregulation of caveolin-1 affects bleomycin-induced growth arrest and cellular senescence in A549 cells. Int. J. Biochem. Cell Biol., 2007, 39(10), 1964-1974.
[118]
Pazolli, E.; Alspach, E.; Milczarek, A.; Prior, J.; Piwnica-worms, D.; Stewart, S.A. Chromatin remodeling underlies the senescence-associated secretory phenotype of tumor stromal fibroblasts that supports cancer progression. Cancer Res., 2012, 72(9), 2251-2261.
[119]
Bearss, D.J.; Hurley, L.H.; Von Hoff, D.D. Telomere maintenance mechanisms as a target for drug development. Oncogene, 2000, 19(56), 6632-6641.
[120]
Multani, A.S.; Furlong, C.; Pathak, S. Reduction of telomeric signals in murine melanoma and human breast cancer cell lines treated with 3′-azido-2′-3′-dideoxythymidine. Int. J. Oncol., 1998, 13(5), 923-925.
[121]
Demir, M.; Laywell, E.D. Neurotoxic effects of AZT on developing and adult neurogenesis. Front. Neurosci., 2015, 9, 93.
[122]
Datta, A.; Bellon, M.; Sinha-Datta, U.; Bazarbachi, A.; Lepelletier, Y.; Canioni, D.; Waldmann, T.A.; Hermine, O.; Nicot, C. Persistent inhibition of telomerase reprograms adult T-cell leukemia to p53-dependent senescence. Blood, 2006, 108(3), 1021-1029.
[123]
Zhou, J.M.; Zhu, X.F.; Lu, Y.J.; Deng, R.; Huang, Z.S.; Mei, Y.P.; Wang, Y.; Huang, W.L.; Liu, Z.C.; Gu, L.Q.; Zeng, Y.X. Senescence and telomere shortening induced by novel potent G-quadruplex interactive agents, quindoline derivatives, in human cancer cell lines. Oncogene, 2006, 25(4), 503-511.
[124]
Huang, F.C.; Chang, C.C.; Wang, J.M.; Chang, T.C.; Lin, J.J. Induction of senescence in cancer cells by the G-quadruplex stabilizer, BMVC4, is independent of its telomerase inhibitory activity. Br. J. Pharmacol., 2012, 167(2), 393-406.
[125]
Muller, S.; Sanders, D.A.; Di Antonio, M.; Matsis, S.; Riou, J.F.; Rodriguez, R.; Balasubramanian, S. Pyridostatin analogues promote telomere dysfunction and long-term growth inhibition in human cancer cells. Org. Biomol. Chem., 2012, 10(32), 6537-6546.
[126]
Riou, J.F.; Guittat, L.; Mailliet, P.; Laoui, A.; Renou, E.; Petitgenet, O.; Megnin-Chanet, F.; Helene, C.; Mergny, J.L. Cell senescence and telomere shortening induced by a new series of specific G-quadruplex DNA ligands. Proc. Natl. Acad. Sci. USA, 2002, 99(5), 2672-2677.
[127]
Taka, T.; Huang, L.; Wongnoppavich, A.; Tam-Chang, S.W.; Lee, T.R.; Tuntiwechapikul, W. Telomere shortening and cell senescence induced by perylene derivatives in A549 human lung cancer cells. Bioorg. Med. Chem., 2013, 21(4), 883-890.
[128]
Zhao, L.; Wink, M. The beta-carboline alkaloid harmine inhibits telomerase activity of MCF-7 cells by down-regulating hTERT mRNA expression accompanied by an accelerated senescent phenotype. PeerJ, 2013, 1, e174.
[129]
Marconett, C.N.; Sundar, S.N.; Tseng, M.; Tin, A.S.; Tran, K.Q.; Mahuron, K.M.; Bjeldanes, L.F.; Firestone, G.L. Indole-3-carbinol downregulation of telomerase gene expression requires the inhibition of estrogen receptor-alpha and Sp1 transcription factor interactions within the hTERT promoter and mediates the G1 cell cycle arrest of human breast cancer cells. Carcinogenesis, 2011, 32(9), 1315-1323.
[130]
Shimizu, H.; Bolati, D.; Adijiang, A.; Muteliefu, G.; Enomoto, A.; Nishijima, F.; Dateki, M.; Niwa, T. NF-kappaB plays an important role in indoxyl sulfate-induced cellular senescence, fibrotic gene expression, and inhibition of proliferation in proximal tubular cells. Am. J. Physiol. Cell Physiol., 2011, 301(5), C1201-C1212.
[131]
Shimizu, H.; Bolati, D.; Adijiang, A.; Enomoto, A.; Nishijima, F.; Dateki, M.; Niwa, T. Senescence and dysfunction of proximal tubular cells are associated with activated p53 expression by indoxyl sulfate. Am. J. Physiol. Cell Physiol., 2010, 299(5), C1110-C1117.
[132]
Damm, K.; Hemmann, U.; Garin-Chesa, P.; Hauel, N.; Kauffmann, I.; Priepke, H.; Niestroj, C.; Daiber, C.; Enenkel, B.; Guilliard, B.; Lauritsch, I.; Muller, E.; Pascolo, E.; Sauter, G.; Pantic, M.; Martens, U.M.; Wenz, C.; Lingner, J.; Kraut, N.; Rettig, W.J.; Schnapp, A. A highly selective telomerase inhibitor limiting human cancer cell proliferation. EMBO J., 2001, 20(24), 6958-6968.
[133]
Yokoyama, Y.; Takahashi, Y.; Shinohara, A.; Wan, X.; Takahashi, S.; Niwa, K.; Tamaya, T. The 5′-end of hTERT mRNA is a good target for hammerhead ribozyme to suppress telomerase activity. Biochem. Biophys. Res. Commun., 2000, 273(1), 316-321.
[134]
Denchi, E.L.; de Lange, T. Protection of telomeres through independent control of ATM and ATR by TRF2 and POT1. Nature, 2007, 448(7157), 1068-1071.
[135]
Vogt, M.; Haggblom, C.; Yeargin, J.; Christiansen-Weber, T.; Haas, M. Independent induction of senescence by p16INK4a and p21CIP1 in spontaneously immortalized human fibroblasts. Cell Growth Differ., 1998, 9(2), 139-146.
[136]
Venturelli, S.; Berger, A.; Weiland, T.; Essmann, F.; Waibel, M.; Nuebling, T.; Hacker, S.; Schenk, M.; Schulze-Osthoff, K.; Salih, H.R.; Fulda, S.; Sipos, B.; Johnstone, R.W.; Lauer, U.M.; Bitzer, M. Differential induction of apoptosis and senescence by the DNA methyltransferase inhibitors 5-azacytidine and 5-aza-2′-deoxycytidine in solid tumor cells. Mol. Cancer Ther., 2013, 12(10), 2226-2236.
[137]
Widodo, N.; Deocaris, C.C.; Kaur, K.; Hasan, K.; Yaguchi, T.; Yamasaki, K.; Sugihara, T.; Ishii, T.; Wadhwa, R.; Kaul, S.C. Stress chaperones, mortalin, and pex19p mediate 5-aza-2′ deoxycytidine-induced senescence of cancer cells by DNA methylation-independent pathway. J. Gerontol. A Biol. Sci. Med. Sci., 2007, 62(3), 246-255.
[138]
Amatori, S.; Bagaloni, I.; Viti, D.; Fanelli, M. Premature senescence induced by DNA demethylating agent (Decitabine) as therapeutic option for malignant pleural mesothelioma. Lung Cancer, 2011, 71(1), 113-115.
[139]
Yuan, Y.; Wang, Q.; Paulk, J.; Kubicek, S.; Kemp, M.M.; Adams, D.J.; Shamji, A.F.; Wagner, B.K.; Schreiber, S.L. A small-molecule probe of the histone methyltransferase G9a induces cellular senescence in pancreatic adenocarcinoma. ACS Chem. Biol., 2012, 7(7), 1152-1157.
[140]
Ogryzko, V.V.; Hirai, T.H.; Russanova, V.R.; Barbie, D.A.; Howard, B.H. Human fibroblast commitment to a senescence-like state in response to histone deacetylase inhibitors is cell cycle dependent. Mol. Cell. Biol., 1996, 16(9), 5210-5218.
[141]
Xiao, H.; Hasegawa, T.; Miyaishi, O.; Ohkusu, K.; Isobe, K. Sodium butyrate induces NIH3T3 cells to senescence-like state and enhances promoter activity of p21WAF/CIP1 in p53-independent manner. Biochem. Biophys. Res. Commun., 1997, 237(2), 457-460.
[142]
Terao, Y.; Nishida, J.; Horiuchi, S.; Rong, F.; Ueoka, Y.; Matsuda, T.; Kato, H.; Furugen, Y.; Yoshida, K.; Kato, K.; Wake, N. Sodium butyrate induces growth arrest and senescence-like phenotypes in gynecologic cancer cells. Int. J. Cancer, 2001, 94(2), 257-267.
[143]
Place, R.F.; Noonan, E.J.; Giardina, C. HDACs and the senescent phenotype of WI-38 cells. BMC Cell Biol., 2005, 6, 37.
[144]
Abramova, M.V.; Pospelova, T.V.; Nikulenkov, F.P.; Hollander, C.M.; Fornace, A.J. Jr.; Pospelov, V.A. G1/S arrest induced by histone deacetylase inhibitor sodium butyrate in E1A + Ras-transformed cells is mediated through down-regulation of E2F activity and stabilization of beta-catenin. J. Biol. Chem., 2006, 281(30), 21040-21051.
[145]
Pospelova, T.V.; Demidenko, Z.N.; Bukreeva, E.I.; Pospelov, V.A.; Gudkov, A.V.; Blagosklonny, M.V. Pseudo-DNA damage response in senescent cells. Cell Cycle, 2009, 8(24), 4112-4118.
[146]
Xu, W.S.; Perez, G.; Ngo, L.; Gui, C.Y.; Marks, P.A. Induction of polyploidy by histone deacetylase inhibitor: a pathway for antitumor effects. Cancer Res., 2005, 65(17), 7832-7839.
[147]
Cain, J.E.; McCaw, A.; Jayasekara, W.S.; Rossello, F.J.; Marini, K.D.; Irving, A.T.; Kansara, M.; Thomas, D.M.; Ashley, D.M.; Watkins, D.N. Sustained low-dose treatment with the histone deacetylase inhibitor LBH589 induces terminal differentiation of osteosarcoma cells. Sarcoma, 2013, 2013, 608964.
[148]
Kim, H.D.; Jang, C.Y.; Choe, J.M.; Sohn, J.; Kim, J. Phenylbutyric acid induces the cellular senescence through an Akt/p21(WAF1) signaling pathway. Biochem. Biophys. Res. Commun., 2012, 422(2), 213-218.
[149]
Li, X.N.; Shu, Q.; Su, J.M.; Perlaky, L.; Blaney, S.M.; Lau, C.C. Valproic acid induces growth arrest, apoptosis, and senescence in medulloblastomas by increasing histone hyperacetylation and regulating expression of p21Cip1, CDK4, and CMYC. Mol. Cancer Ther., 2005, 4(12), 1912-1922.
[150]
An, H.M.; Xue, Y.F.; Shen, Y.L.; Du, Q.; Hu, B. Sodium valproate induces cell senescence in human hepatocarcinoma cells. Molecules, 2013, 18(12), 14935-14947.
[151]
Di Bernardo, G.; Squillaro, T.; Dell’Aversana, C.; Miceli, M.; Cipollaro, M.; Cascino, A.; Altucci, L.; Galderisi, U. Histone deacetylase inhibitors promote apoptosis and senescence in human mesenchymal stem cells. Stem Cells Dev., 2009, 18(4), 573-581.
[152]
Mosieniak, G.; Adamowicz, M.; Alster, O.; Jaskowiak, H.; Szczepankiewicz, A.A.; Wilczynski, G.M.; Ciechomska, I.A.; Sikora, E. Curcumin induces permanent growth arrest of human colon cancer cells: link between senescence and autophagy. Mech. Ageing Dev., 2012, 133(6), 444-455.
[153]
Hendrayani, S.F.; Al-Khalaf, H.H.; Aboussekhra, A. Curcumin triggers p16-dependent senescence in active breast cancer-associated fibroblasts and suppresses their paracrine procarcinogenic effects. Neoplasia, 2013, 15(6), 631-640.
[154]
Grabowska, W.; Kucharewicz, K.; Wnuk, M.; Lewinska, A.; Suszek, M.; Przybylska, D.; Mosieniak, G.; Sikora, E.; Bielak-Zmijewska, A. Curcumin induces senescence of primary human cells building the vasculature in a DNA damage and ATM-independent manner. Age (Dordr.), 2015, 37(1), 9744.
[155]
Gewirtz, D.A.; Holt, S.E.; Elmore, L.W. Accelerated senescence: an emerging role in tumor cell response to chemotherapy and radiation. Biochem. Pharmacol., 2008, 76(8), 947-957.
[156]
Klein, L.E.; Freeze, B.S.; Smith, A.B. 3rd.; Horwitz, S.B. The microtubule stabilizing agent discodermolide is a potent inducer of accelerated cell senescence. Cell Cycle, 2005, 4(3), 501-507.
[157]
Arthur, C.R.; Gupton, J.T.; Kellogg, G.E.; Yeudall, W.A.; Cabot, M.C.; Newsham, I.F.; Gewirtz, D.A. Autophagic cell death, polyploidy and senescence induced in breast tumor cells by the substituted pyrrole JG-03-14, a novel microtubule poison. Biochem. Pharmacol., 2007, 74(7), 981-991.
[158]
Tierno, M.B.; Kitchens, C.A.; Petrik, B.; Graham, T.H.; Wipf, P.; Xu, F.L.; Saunders, W.S.; Raccor, B.S.; Balachandran, R.; Day, B.W.; Stout, J.R.; Walczak, C.E.; Ducruet, A.P.; Reese, C.E.; Lazo, J.S. Microtubule binding and disruption and induction of premature senescence by disorazole C(1). J. Pharmacol. Exp. Ther., 2009, 328(3), 715-722.
[159]
Chan, A.; Gilfillan, C.; Templeton, N.; Paterson, I.; Northcote, P.T.; Miller, J.H. Induction of accelerated senescence by the microtubule-stabilizing agent peloruside A. Invest. New Drugs, 2017, 35(6), 706-717.
[160]
Chao, S.K.; Lin, J.; Brouwer-Visser, J.; Smith, A.B., III; Horwitz, S.B.; McDaid, H.M. Resistance to discodermolide, a microtubule-stabilizing agent and senescence inducer, is 4E-BP1-dependent. Proc. Natl. Acad. Sci. USA, 2011, 108(1), 391-396.
[161]
Duan, L.; Sterba, K.; Kolomeichuk, S.; Kim, H.; Brown, P.H.; Chambers, T.C. Inducible overexpression of c-Jun in MCF7 cells causes resistance to vinblastine via inhibition of drug-induced apoptosis and senescence at a step subsequent to mitotic arrest. Biochem. Pharmacol., 2007, 73(4), 481-490.
[162]
Volpp, K.G.; John, L.K.; Troxel, A.B.; Norton, L.; Fassbender, J.; Loewenstein, G. Financial incentive-based approaches for weight loss: a randomized trial. JAMA, 2008, 300(22), 2631-2637.
[163]
Campisi, J. Cellular senescence: putting the paradoxes in perspective. Curr. Opin. Genet. Dev., 2011, 21(1), 107-112.
[164]
Laberge, R.M.; Zhou, L.; Sarantos, M.R.; Rodier, F.; Freund, A.; de Keizer, P.L.; Liu, S.; Demaria, M.; Cong, Y.S.; Kapahi, P.; Desprez, P.Y.; Hughes, R.E.; Campisi, J. Glucocorticoids suppress selected components of the senescence-associated secretory phenotype. Aging Cell, 2012, 11(4), 569-578.
[165]
Lim, H.; Park, H.; Kim, H.P. Effects of flavonoids on senescence-associated secretory phenotype formation from bleomycin-induced senescence in BJ fibroblasts. Biochem. Pharmacol., 2015, 96(4), 337-348.
[166]
Braig, M.; Lee, S.; Loddenkemper, C.; Rudolph, C.; Peters, A.H.; Schlegelberger, B.; Stein, H.; Dorken, B.; Jenuwein, T.; Schmitt, C.A. Oncogene-induced senescence as an initial barrier in lymphoma development. Nature, 2005, 436(7051), 660-665.
[168]
Chien, Y.; Scuoppo, C.; Wang, X.; Fang, X.; Balgley, B.; Bolden, J.E.; Premsrirut, P.; Luo, W.; Chicas, A.; Lee, C.S.; Kogan, S.C.; Lowe, S.W. Control of the senescence-associated secretory phenotype by NF-kappaB promotes senescence and enhances chemosensitivity. Genes Dev., 2011, 25(20), 2125-2136.
[170]
Giancotti, F.G. Mechanisms governing metastatic dormancy and reactivation. Cell, 2013, 155(4), 750-764.
[171]
Milanovic, M.; Fan, D.N.Y.; Belenki, D.; Dabritz, J.H.M.; Zhao, Z.; Yu, Y.; Dorr, J.R.; Dimitrova, L.; Lenze, D.; Monteiro Barbosa, I.A.; Mendoza-Parra, M.A.; Kanashova, T.; Metzner, M.; Pardon, K.; Reimann, M.; Trumpp, A.; Dorken, B.; Zuber, J.; Gronemeyer, H.; Hummel, M.; Dittmar, G.; Lee, S.; Schmitt, C.A. Senescence-associated reprogramming promotes cancer stemness. Nature, 2018, 553(7686), 96.
Related Books
Frontiers in Clinical Drug Research - Anti-Cancer Agents
NEOPLASIA and FERTILITY
Breast Cancer: Current Trends in Molecular Research
The Evolution of Radionanotargeting towards Clinical Precision Oncology: A Festschrift in Honor of Kalevi Kairemo
Nanotherapeutics for the Treatment of Hepatocellular Carcinoma
Topics in Anti-Cancer Research
Frontiers in Clinical Drug Research - Anti-Cancer Agents
Modern Cancer Therapies and Traditional Medicine: An Integrative Approach to Combat Cancers
Herbal Medicine: Back to the Future
Thrombosis in Cancer: A Medical Professional's Guide to Cancer Associated Thrombosis
Article Metrics
88
10