Cytokine expression and signaling in drug-induced cellular senescence

0333900 - ÚMG 2010 RIV GB eng J - Journal Article
Nováková, Zora - Hubáčková, Soňa - Košař, Martin - Janderová-Rossmeislová, Lenka - Dobrovolná, Jana - Vašicová, Pavla - Vančurová, Markéta - Hořejší, Zuzana - Hozák, Pavel - Bártek, Jiří - Hodný, Zdeněk
Cytokine expression and signaling in drug-induced cellular senescence.
Oncogene. Roč. 29, č. 2 (2010), s. 273-284. ISSN 0950-9232. E-ISSN 1476-5594
R&D Projects: GA AV ČR IAA500390501; GA ČR GA204/08/1418; GA MŠMT LC545
Grant - others:EC(XE) TRIREME
Institutional research plan: CEZ:AV0Z50520514; CEZ:AV0Z50200510
Keywords : cellular senescence * cytokines * JAK/STAT signaling pathway
Subject RIV: EB - Genetics ; Molecular Biology
Impact factor: 7.414, year: 2010

Cellular senescence, the permanent state of cell-cycle arrest, is emerging as an intrinsic barrier against tumorigenesis and a mechanism contributing to organismal ageing. Pathophysiologically relevant part of senescent phenotype is the expression and secretion of several cytokines. In this article we present that premature cellular senescence promoted by senescence-inducing compounds (e.g. bromodeoxyuridine, distamycin A, hydroxyurea, and aphidicoline) in several human tumor cell lines is accompanied by persistent activity of the interferon JAK/STAT signaling pathway and the expression of several interferon-stimulated genes such as MX1, OAS, ISG15, STAT1, PML, IRF1 and IRF7. JAK1/STAT-activating ligands IL-10, IL-20, IL-24, IFNgamma, IFNbeta and IL-6 were also expressed by senescent cells, supporting autocrine/paracrine activation of JAK1/STAT. Furthermore, cytokine genes including proinflammatory IL-1, TNF and TGF families were highly expressed.
Permanent Link: http://hdl.handle.net/11104/0178775