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Senescent cells develop a parp-1 and nuclear factor-κB-associated secretome (PNAS).
Open accessAbstract
Melanoma cells can enter the process of senescence, but whether they express a secretory phenotype, as reported for other cells, is undetermined. This is of paramount importance, because this secretome can alter the tumor microenvironment and the response to chemotherapeutic drugs. More generally, the molecular events involved in formation of the senescent-associated secretome have yet to be determined. We reveal here that melanoma cells experiencing senescence in response to diverse stimuli, including anti-melanoma drugs, produce an inflammatory secretory profile, where the chemokine ligand-2 (CCL2) acts as a critical effector. Thus, we reveal how senescence induction might be involved in therapeutic failure in melanoma. We further provide a molecular relationship between senescence induction and secretome formation by revealing that the poly(ADP-ribose) polymerase-1 (PARP-1)/nuclear factor-κB (NF-κB) signaling cascade, activated during senescence, drives the formation of a secretome endowed with protumoral and prometastatic properties. Our findings also point to the existence of the PARP-1 and NF-κB-associated secretome, termed the PNAS, in nonmelanoma cells. Most importantly, inhibition of PARP-1 or NF-κB prevents the proinvasive properties of the secretome. Collectively, identification of the PARP-1/NF-κB axis in secretome formation opens new avenues for therapeutic intervention against cancers.
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“Blocking PARP-1, ATM, or NF-κB in melanoma cells prevents the secretion of chemokine CCL2 thereby restricting the deleterious pro-invasive properties of the inflammatory SASP mediated by PNAS (Ohanna et al., 2011).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Ohanna et al., 2011
In the citing paper
“Chemotherapeutic drugs or oxidative stress induced DNA damage engage PARP-1/ATM/NF-κB signaling cascade to induce senescence in melanoma and non-melanoma cells (Ohanna et al., 2011).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Ohanna et al., 2011
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“These senescent cells develop a PARP-1 and NF-κB associated secretome (PNAS) containing chemokine CCL2 along with other SASP factors thereby augmenting the invasiveness of melanoma cells which might have escaped senescence.”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Ohanna et al., 2011
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“some tumor cells can enter senescence in response to DNA damaging therapies [363,364].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [364]
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1 retracted
Ionizing radiation-induced NF-κB activation requires PARP-1 function to confer radioresistance
Veuger, S. J., Hunter, J. E., & Durkacz, B. W. (2008) · Oncogene · doi:10.1038/onc.2008.439 · Cited by 134
RetractedOncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218 · cited 1×
“Ordinarily, senescence is a process arising in normal cells in response to telomere erosion or oncogenic stress, acting through checkpoint activation and cell cycle arrest as a barrier to tumorigenesis (Serrano et al. 1997; Steinert et al. 2000).”
BackgroundThe senescence-associated secretory phenotype: the dark side of tumor suppression
Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102144 · Cited by 5,206
The Nuclear Factor NF- B Pathway in InflammationPreprint
Lawrence, T. (2009) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a001651 · Cited by 5,126
Hartwell, L. H., & Kastan, M. B. (1994) · Science · doi:10.1126/science.7997877 · Cited by 2,539
Oncogene-Induced Senescence Relayed by an Interleukin-Dependent Inflammatory Network
Kuilman, T., Michaloglou, C., Vredeveld, L. C. W., Douma, S., van Doorn, R., Desmet, C. J., Aarden, L. A., Mooi, W. J., & Peeper, D. S. (2008) · Cell · doi:10.1016/j.cell.2008.03.039 · Cited by 2,086
Cell Cycle Checkpoints: Preventing an Identity Crisis
Elledge, S. J. (1996) · Science · doi:10.1126/science.274.5293.1664 · Cited by 2,050
Chemokine signaling via the CXCR2 receptor reinforces senescence
Acosta, J. C., O'Loghlen, A., Banito, A., Guijarro, M. V., Augert, A., Raguz, S., Fumagalli, M., Da Costa, M., Brown, C., Popov, N., et al. (2008) · Cell · doi:10.1016/j.cell.2008.03.038 · Cited by 1,801 · cited 1×
“Some of these factors display cell-autonomous activity and work to reinforce the senescence program (Acosta et al. 2008; Kuilman et al. 2008).”
BackgroundKrtolica, A., Parrinello, S., Lockett, S., Desprez, P.-Y., & Campisi, J. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.211053698 · Cited by 1,730
DNA repair pathways as targets for cancer therapy
Helleday, T., Petermann, E., Lundin, C., Hodgson, B., & Sharma, R. A. (2008) · Nature Reviews Cancer · doi:10.1038/nrc2342 · Cited by 1,666
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Hallmarks of Cellular Senescence
Hernandez-Segura, A., Nehme, J., & Demaria, M. (2018) · Trends in Cell Biology · doi:10.1016/j.tcb.2018.02.001 · Cited by 2,605
Cellular senescence in aging and age-related disease: from mechanisms to therapy
Childs, B. G., Durik, M., Baker, D. J., & van Deursen, J. M. (2015) · Nature Medicine · doi:10.1038/nm.4000 · Cited by 2,363
Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype
Kumari, R., & Jat, P. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.645593 · Cited by 1,622
The senescence-associated secretory phenotype and its physiological and pathological implications
Wang, B., Han, J., Elisseeff, J. H., & Demaria, M. (2024) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-024-00727-x · Cited by 948
Senescence and cancer — role and therapeutic opportunities
Schmitt, C. A., Wang, B., & Demaria, M. (2022) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-022-00668-4 · Cited by 794
On PAR with PARP: cellular stress signaling through poly(ADP-ribose) and PARP-1Preprint
Luo, X., & Kraus, W. L. (2012) · Genes & Development · doi:10.1101/gad.183509.111 · Cited by 759
The metabolic roots of senescence: mechanisms and opportunities for intervention
Wiley, C. D., & Campisi, J. (2021) · Nature Metabolism · doi:10.1038/s42255-021-00483-8 · Cited by 691
Moiseeva, O., Deschênes‐Simard, X., St‐Germain, E., Igelmann, S., Huot, G., Cadar, A. E., Bourdeau, V., Pollak, M. N., & Ferbeyre, G. (2013) · Aging Cell · doi:10.1111/acel.12075 · Cited by 654
The dynamic nature of senescence in cancer
Lee, S., & Schmitt, C. A. (2019) · Nature Cell Biology · doi:10.1038/s41556-018-0249-2 · Cited by 588
Targeting the CCL2-CCR2 signaling axis in cancer metastasis
Lim, S. Y., Yuzhalin, A. E., Gordon-Weeks, A. N., & Muschel, R. J. (2016) · Oncotarget · doi:10.18632/oncotarget.7376 · Cited by 515
From Ancient Pathways to Aging Cells—Connecting Metabolism and Cellular Senescence
Wiley, C. D., & Campisi, J. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2016.05.010 · Cited by 440
SUMO and the robustness of cancer
Seeler, J.-S., & Dejean, A. (2017) · Nature reviews. Cancer · doi:10.1038/nrc.2016.143 · Cited by 443
Goding, C. R., & Arnheiter, H. (2019) · Genes & Development · doi:10.1101/gad.324657.119 · Cited by 430
Mechanisms and Regulation of Cellular Senescence
Roger, L., Tomas, F., & Gire, V. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222313173 · Cited by 395
Phenotype plasticity as enabler of melanoma progression and therapy resistance
Arozarena, I., & Wellbrock, C. (2019) · Nature Reviews Cancer · doi:10.1038/s41568-019-0154-4 · Cited by 381
Takahashi, A., Loo, T. M., Okada, R., Kamachi, F., Watanabe, Y., Wakita, M., Watanabe, S., Kawamoto, S., Miyata, K., Barber, G. N., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-03555-8 · Cited by 350
Pluquet, O., Pourtier, A., & Abbadie, C. (2015) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00334.2014 · Cited by 305
Cuollo, L., Antonangeli, F., Santoni, A., & Soriani, A. (2020) · Biology · doi:10.3390/biology9120485 · Cited by 291
DNA damage‐dependent NF‐κB activation: NEMO turns nuclear signaling inside out
McCool, K. W., & Miyamoto, S. (2012) · Immunological Reviews · doi:10.1111/j.1600-065x.2012.01101.x · Cited by 253
Beyond DNA Repair: Additional Functions of PARP-1 in Cancer
Weaver, A. N., & Yang, E. S. (2013) · Frontiers in Oncology · doi:10.3389/fonc.2013.00290 · Cited by 246
Malaquin, N., Martinez, A., & Rodier, F. (2016) · Experimental Gerontology · doi:10.1016/j.exger.2016.05.010 · Cited by 247
Riesenberg, S., Groetchen, A., Siddaway, R., Bald, T., Reinhardt, J., Smorra, D., Sirokay, J. D., Renn, M., Phung, B., Aymans, P., et al. (2015) · Nature Communications · doi:10.1038/ncomms9755 · Cited by 238
Emerging roles of extracellular vesicles in cellular senescence and aging
Takasugi, M. (2018) · Aging Cell · doi:10.1111/acel.12734 · Cited by 227
Pathways and therapeutic targets in melanoma
Shtivelman, E., Davies, M. A., Hwu, P., Yang, J. C.-H., Lotem, M., Oren, M., Flaherty, K. T., & Fisher, D. E. (2014) · Oncotarget · doi:10.18632/oncotarget.1892 · Cited by 226
SASP: Tumor Suppressor or Promoter? Yes!
Rao, S. G., & Jackson, J. G. (2016) · Trends in Cancer · doi:10.1016/j.trecan.2016.10.001 · Cited by 206
Chen, H., Ruiz, P. D., McKimpson, W. M., Novikov, L., Kitsis, R. N., & Gamble, M. J. (2015) · Molecular Cell · doi:10.1016/j.molcel.2015.07.011 · Cited by 205
Heterogeneous Tumor Subpopulations Cooperate to Drive Invasion
Chapman, A., del Ama, L. F., Ferguson, J., Kamarashev, J. A., Wellbrock, C., & Hurlstone, A. F. L. (2014) · Cell Reports · doi:10.1016/j.celrep.2014.06.045 · Cited by 195
Laurette, P., Strub, T., Koludrović, D., Keime, C., Gras, S. L., Seberg, H., Otterloo, E. V., Imrichová, H., Siddaway, R., Aerts, S., et al. (2015) · eLife · doi:10.7554/elife.06857 · Cited by 203
Metabolic landscape in cardiac aging: insights into molecular biology and therapeutic implications
Xie, S., Xu, S., Deng, W., & Tang, Q. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01378-8 · Cited by 197
Bent, E. H., Gilbert, L. A., & Hemann, M. T. (2016) · Genes & Development · doi:10.1101/gad.284851.116 · Cited by 179
SIRT1 suppresses the senescence-associated secretory phenotype through epigenetic gene regulation
Hayakawa, T., Iwai, M., Aoki, S., Takimoto, K., Maruyama, M., Maruyama, W., & Motoyama, N. (2015) · PLOS ONE · doi:10.1371/journal.pone.0116480 · Cited by 170
“Social Life” of Senescent Cells: What Is SASP and Why Study It?
Borodkina, A. V., Deryabin, P. I., Giukova, А. А., & Nikolsky, N. N. (2018) · Acta Naturae · doi:10.32607/20758251-2018-10-1-4-14 · Cited by 170
Cellular Senescence: From Mechanisms to Current Biomarkers and Senotherapies
Lucas, V., Cavadas, C., & Aveleira, C. A. (2023) · Pharmacological Reviews · doi:10.1124/pharmrev.122.000622 · Cited by 172
Cell Senescence, DNA Damage, and Metabolism
Shmulevich, R., & Krizhanovsky, V. (2021) · Antioxidants & Redox Signaling · doi:10.1089/ars.2020.8043 · Cited by 157
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Simiczyjew, A., Dratkiewicz, E., Mazurkiewicz, J., Ziętek, M., Matkowski, R., & Nowak, D. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21218359 · Cited by 157
The role of cellular senescence and SASP in tumour microenvironment
Takasugi, M., Yoshida, Y., Hara, E., & Ohtani, N. (2023) · The FEBS Journal · doi:10.1111/febs.16381 · Cited by 144
Ali, T. H., Pisanti, S., Ciaglia, E., Mortarini, R., Anichini, A., Garofalo, C., Tallerico, R., Santinami, M., Gulletta, E., Ietto, C., et al. (2014) · Nature Communications · doi:10.1038/ncomms6639 · Cited by 145
Perspectives on translational and therapeutic aspects of SIRT1 in inflammaging and senescence
Yao, H., & Rahman, I. (2012) · Biochemical Pharmacology · doi:10.1016/j.bcp.2012.06.031 · Cited by 141
Beyond Cell Motility: The Expanding Roles of Chemokines and Their Receptors in Malignancy
Morein, D., Erlichman, N., & Ben‐Baruch, A. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.00952 · Cited by 138
Melanoma: From Melanocyte to Genetic Alterations and Clinical Options
Bertolotto, C. (2013) · Scientifica · doi:10.1155/2013/635203 · Cited by 152
Self-citationRole of Cellular Senescence in Type II Diabetes
Narasimhan, A., Flores, R. R., Robbins, P. D., & Niedernhofer, L. J. (2021) · Endocrinology · doi:10.1210/endocr/bqab136 · Cited by 133
Cellular Interactions in the Tumor Microenvironment: The Role of Secretome
da Cunha, B. R., Domingos, C., Stefanini, A. C. B., Henrique, T., Polachini, G. M., Castelo‐Branco, P., & Tajara, E. H. (2019) · Journal of Cancer · doi:10.7150/jca.21780 · Cited by 133
Mangerich, A., & Bürkle, A. (2012) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2012/321653 · Cited by 133
Roles and mechanisms of cellular senescence in regulation of tissue homeostasis
Ohtani, N., & Hara, E. (2013) · Cancer Science · doi:10.1111/cas.12118 · Cited by 122
DDR-mediated crosstalk between DNA-damaged cells and their microenvironment
Malaquin, N., Carrier-Leclerc, A., Dessureault, M., & Rodier, F. (2015) · Frontiers in Genetics · doi:10.3389/fgene.2015.00094 · Cited by 124
PARP-1: Friend or Foe of DNA Damage and Repair in Tumorigenesis?
Swindall, A. F., Stanley, J. A., & Yang, E. S.-H. (2013) · Cancers · doi:10.3390/cancers5030943 · Cited by 123
Bai, X., Fisher, D. E., & Flaherty, K. T. (2019) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-019-0204-6 · Cited by 107
Cellular senescence: a promising strategy for cancer therapy
Lee, S., & Lee, J. (2019) · BMB Reports · doi:10.5483/bmbrep.2019.52.1.294 · Cited by 117
Polyphenols as Caloric-Restriction Mimetics and Autophagy Inducers in Aging Research
Yessenkyzy, A., Saliev, T. M., Zhanaliyeva, M., Masoud, A., Umbayev, B. A., Sergazy, S., Кривых, Е. А., Gulyayev, A., & Nurgozhin, T. S. (2020) · Nutrients · doi:10.3390/nu12051344 · Cited by 119
Vemurafenib Induces Senescence Features in Melanoma Cells
Haferkamp, S., Borst, A., Adam, C., Becker, T. M., Motschenbacher, S., Windhövel, S., Hufnagel, A., Houben, R., & Meierjohann, S. (2013) · Journal of Investigative Dermatology · doi:10.1038/jid.2013.6 · Cited by 116
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Yao, H., & Rahman, I. (2012) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00175.2012 · Cited by 109
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Focus on cutaneous and uveal melanoma specificitiesPreprint
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Self-citationPandiani, C., Strub, T., Nottet, N., Chéli, Y., Gambi, G., Bille, K., Husser, C., Dalmasso, M., Béranger, G. E., Lassalle, S., et al. (2021) · Cell Death and Differentiation · doi:10.1038/s41418-020-00730-7 · Cited by 103
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Hua, J., Kase, J., Dörr, J. R., Milanovic, M., Lenze, D., Grau, M., Beuster, G., Ji, S., Reimann, M., Lenz, P., et al. (2011) · Genes & Development · doi:10.1101/gad.17620611 · Cited by 102
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Rossi, A., Roberto, M., Panebianco, M., Botticelli, A., Mazzuca, F., & Marchetti, P. (2019) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2019.172621 · Cited by 95
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Meng, Y., Efimova, E. V., Hamzeh, K., Darga, T. E., Mauceri, H. J., Fu, Y., Kron, S. J., & Weichselbaum, R. R. (2012) · Molecular Therapy · doi:10.1038/mt.2012.19 · Cited by 97
Sun, X., Shi, B., Zheng, H., Min, L., Yang, J., Li, X., Liao, X., Huang, W., Zhang, M., Xu, S., et al. (2018) · Cell Death and Disease · doi:10.1038/s41419-018-0303-9 · Cited by 95
Ohanna, M., Cerezo, M., Nottet, N., Bille, K., Didier, R., Béranger, G. E., Mograbi, B., Rocchi, S., Yvan‐Charvet, L., Ballotti, R., et al. (2018) · Genes & Development · doi:10.1101/gad.305854.117 · Cited by 97
Self-citationCancer secretome and inflammation: The bright and the dark sides of NF-κB
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Vaughan, S., & Jat, P. (2011) · Aging · doi:10.18632/aging.100390 · Cited by 90
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Zhang, H., Xu, J., Long, Y., Maimaitijiang, A., Su, Z., Li, W., & Li, J. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252312928 · Cited by 97
Ohanna, M., Cheli, Y., Bonet, C., Bonazzi, V. F., Allegra, M., Giuliano, S., Bille, K., Bahadoran, P., Giacchero, D., Lacour, J. P., et al. (2013) · Oncotarget · doi:10.18632/oncotarget.1143 · Cited by 78
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Boussios, S., Karathanasi, A., Cooke, D., Neille, C., Sadauskaite, A., Moschetta, M., Zakynthinakis-Kyriakou, N., & Pavlidis, N. A. (2019) · Diagnostics · doi:10.3390/diagnostics9020055 · Cited by 80
Hu, Q., Peng, J., Jiang, L., Li, W., Su, Q., Zhang, J., Li, H., Song, M., Cheng, B., Xia, J., et al. (2020) · Cell Death and Disease · doi:10.1038/s41419-020-03126-0 · Cited by 78
Bonet, C., Giuliano, S., Ohanna, M., Bille, K., Allégra, M., Lacour, J. ‐., Bahadoran, P., Rocchi, S., Ballotti, R., & Bertolotto, C. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.371682 · Cited by 80
Self-citationInflammation-Induced Plasticity in Melanoma Therapy and Metastasis
Hölzel, M., & Tüting, T. (2016) · Trends in Immunology · doi:10.1016/j.it.2016.03.009 · Cited by 80
In vitro evidence for senescent multinucleated melanocytes as a source for tumor-initiating cells
Leikam, C., Hufnagel, A., Otto, C., Murphy, D. J., Mühling, B., Kneitz, S., Nanda, I., Schmid, M., Wagner, T. U., Haferkamp, S., et al. (2015) · Cell Death and Disease · doi:10.1038/cddis.2015.71 · Cited by 76
Epithelial cell senescence: an adaptive response to pre-carcinogenic stresses?
Abbadie, C., Pluquet, O., & Pourtier, A. (2017) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-017-2587-9 · Cited by 77
Sasaki, M., Miyakoshi, M., Sato, Y., & Nakanuma, Y. (2013) · Digestive Diseases and Sciences · doi:10.1007/s10620-013-2920-6 · Cited by 75
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Sun, Y., & Nelson, P. S. (2012) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-11-0768 · Cited by 74
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Blander, H. D., Morel, A., Senaratne, A. P., Ouzounova, M., & Puisieux, A. (2021) · Cancers · doi:10.3390/cancers13184561 · Cited by 82
Ohtani, N. (2014) · Seminars in Immunopathology · doi:10.1007/s00281-014-0457-1 · Cited by 76
Shan, H., Li, T., Zhang, L., Yang, R., Li, Y., Zhang, M., Dong, Y., Zhou, Y., Xu, C., Yang, B., et al. (2018) · EBioMedicine · doi:10.1016/j.ebiom.2018.11.056 · Cited by 75
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Strub, T., Ballotti, R., & Bertolotto, C. (2020) · Theranostics · doi:10.7150/thno.36218 · Cited by 73
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Marjanović, M. P., Crawford, K., & Ahel, I. (2016) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2016.09.014 · Cited by 72
Hadri, K. E., Smith, R., Duplus, E., & Amri, C. E. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms23010077 · Cited by 71
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Self-citation
Metadata
- Authors
- Ohanna, M., Giuliano, S., Bonet, C., Imbert, V., Hofman, V., Zangari, J., Bille, K., Robert, C., Bressac-de Paillerets, B., Hofman, P., Rocchi, S., Peyron, J.-F., Lacour, J.-P., Ballotti, R., & Bertolotto, C.
- Affiliations
- Inserm (FR)
- Institut Gustave Roussy (FR)
- Centre Hospitalier Universitaire de Nice (FR)
- ORCID
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2011-06-06
- Volume
- 25
- Issue
- 12
- Pages
- 1245-1261
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC3127427
- OpenAlex
- W2162942873
- Cited by
- 267
- References
- 67
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 17 · 2023: 24 · 2022: 20 · 2021: 33 · 2020: 25 · 2019: 15 · 2018: 16 · 2017: 13 · 2016: 16 · 2015: 17 · 2014: 13 · 2013: 21 · 2012: 15
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Association pour la Recherche sur le Cancer
- Institut National de la Santé et de la Recherche Médicale
- Fondation de France
- Institut National Du Cancer
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- cellular senescence, senescence-associated secretome, melanoma, PARP1, NF-κB signaling, MCP-1, chemokines, tumor microenvironment, chemoresistance, metastasis, tumor invasion
- MeSH terms
- Poly (ADP-Ribose) Polymerase-1, DNA Damage, Humans, Melanoma, Neoplasm Invasiveness, Poly(ADP-ribose) Polymerases, Signal Transduction, Gene Expression Regulation, Neoplastic, NF-kappa B, Cellular Senescence, Chemokine CCL2, Gene Expression Profiling, Cell Line, Tumor
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