Senescence and immortality in hepatocellular carcinoma

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dc.citation.epage113en_US
dc.citation.issueNumber1en_US
dc.citation.spage103en_US
dc.citation.volumeNumber286en_US
dc.contributor.authorOzturk, M.en_US
dc.contributor.authorArslan-Ergul, A.en_US
dc.contributor.authorBagislar, S.en_US
dc.contributor.authorSenturk, S.en_US
dc.contributor.authorYuzugullu, H.en_US
dc.date.accessioned2015-07-28T11:58:35Z
dc.date.available2015-07-28T11:58:35Z
dc.date.issued2009-10-01en_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.description.abstractCellular senescence is a process leading to terminal growth arrest with characteristic morphological features. This process is mediated by telomere-dependent, oncogene-induced and ROS-induced pathways, but persistent DNA damage is the most common cause. Senescence arrest is mediated by p16(INK4a)- and p21(Cip1)-dependent pathways both leading to retinoblastoma protein (pRb) activation. p53 plays a relay role between DNA damage sensing and p21(Cip1) activation. pRb arrests the cell cycle by recruiting proliferation genes to facultative heterochromatin for permanent silencing. Replicative senescence that occurs in hepatocytes in culture and in liver cirrhosis is associated with lack of telomerase activity and results in telomere shortening. Hepatocellular carcinoma (HCC) cells display inactivating mutations of p53 and epigenetic silencing of p16(INK4a). Moreover, they re-express telomerase reverse transcriptase required for telomere maintenance. Thus, senescence bypass and cellular immortality is likely to contribute significantly to HCC development. Oncogene-induced senescence in premalignant lesions and reversible immortality of cancer cells including HCC offer new potentials for tumor prevention and treatment. (C) 2008 Elsevier Ireland Ltd. All rights reserved.en_US
dc.description.provenanceMade available in DSpace on 2015-07-28T11:58:35Z (GMT). No. of bitstreams: 1 10.1016-j.canlet.2008.10.048.pdf: 330775 bytes, checksum: 8bfc7923fea9da217e8305a8fb57fa97 (MD5)en
dc.identifier.doi10.1016/j.canlet.2008.10.048en_US
dc.identifier.issn0304-3835
dc.identifier.urihttp://hdl.handle.net/11693/11727
dc.language.isoEnglishen_US
dc.publisherElsevieren_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.canlet.2008.10.048en_US
dc.source.titleCancer Lettersen_US
dc.subjectLiver Canceren_US
dc.subjectSenescenceen_US
dc.subjectTelomeresen_US
dc.subjectDna Damageen_US
dc.subjectP53en_US
dc.subjectP16(ink4a)en_US
dc.subjectP21(cip1)en_US
dc.subjectRetinoblastomaen_US
dc.subjectCirrhosisen_US
dc.subjectHepatocytesen_US
dc.subjectTelomerase Reverse Transcriptaseen_US
dc.subjectOncogene-induced Senescenceen_US
dc.subjectHepatitis-b-virusen_US
dc.subjectChronic Liver-diseaseen_US
dc.subjectHuman Tumor-cellsen_US
dc.subjectReplicative Senescenceen_US
dc.subjectCellular Senescenceen_US
dc.subjectUp-regulationen_US
dc.subjectDna-damageen_US
dc.subjectHeterochromatin Formationen_US
dc.subjectTelomere Dysfunctionen_US
dc.titleSenescence and immortality in hepatocellular carcinomaen_US
dc.typeArticleen_US

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