Oncogene-Induced Senescence (OIS) as a Cellular Response to Oncogenic Stresses

作者: Véronique Bourdeau , Gerardo Ferbeyre

DOI: 10.1007/978-1-4419-1075-2_3

关键词: Downregulation and upregulationCell biologySenescenceKinaseSuppressorChemistryPromyelocytic leukemia proteinDNA replicationDNA damageCyclin-dependent kinase

摘要: Oncogene-Induced Senescence (OIS) is a tumor suppressor mechanism that prevents the expansion of cells bearing activated oncogenes. Two major suppressors control OIS: p53 and Rb. These are not to regulate senescence by normal growth signals, but stress signals caused The activation oncogenes involves reactive oxygen species (oxidative stress), DNA replication damage response. Rb during OIS less understood, it Cyclin-Dependent Kinases (CDKs) inhibitors such as p21 p16INK4a or downregulation CDK4, due decrease in Myc functions. also controls formation heterochromatin senescent cells, this process has been linked p16INK4a, promyelocytic leukemia protein PML. occurs both rodents humans, its differ between these species. In rodents, can be inactivated disabling pathway. contrast, human organize Rb-independent senescence. initiated cell autonomous response oncogenes, secreted cytokines. mechanistic understanding suggests novel strategies treat cancers.

参考文章(150)
D Wynford-Thomas, F Wyllie, J Blaydes, V Gire, M Haughton, J Bond, Evidence that transcriptional activation by p53 plays a direct role in the induction of cellular senescence. Oncogene. ,vol. 13, pp. 2097- 2104 ,(1996)
T Christiansen-Weber, J Yeargin, M Vogt, M Haas, C Haggblom, Independent induction of senescence by p16INK4a and p21CIP1 in spontaneously immortalized human fibroblasts Cell Growth & Differentiation. ,vol. 9, pp. 139- 146 ,(1998)
Mark Pearson, Roberta Carbone, Carla Sebastiani, Mario Cioce, Marta Fagioli, Shin’ichi Saito, Yuichiro Higashimoto, Ettore Appella, Saverio Minucci, Pier Paolo Pandolfi, Pier Giuseppe Pelicci, PML regulates p53 acetylation and premature senescence induced by oncogenic Ras Nature. ,vol. 406, pp. 207- 210 ,(2000) , 10.1038/35018127
Daniel S. Peeper, Jan-Hermen Dannenberg, Sirith Douma, Hein te Riele, René Bernards, Escape from premature senescence is not sufficient for oncogenic transformation by Ras Nature Cell Biology. ,vol. 3, pp. 198- 203 ,(2001) , 10.1038/35055110
Ignacio Palmero, Cristina Pantoja, Manuel Serrano, p19ARF links the tumour suppressor p53 to Ras Nature. ,vol. 395, pp. 125- 126 ,(1998) , 10.1038/25870
William C. Hahn, Christopher M. Counter, Ante S. Lundberg, Roderick L. Beijersbergen, Mary W. Brooks, Robert A. Weinberg, Creation of human tumour cells with defined genetic elements Nature. ,vol. 400, pp. 464- 468 ,(1999) , 10.1038/22780
Amancio Carnero, James D. Hudson, Cathy M. Price, David H. Beach, p16INK4A and p19ARF act in overlapping pathways in cellular immortalization. Nature Cell Biology. ,vol. 2, pp. 148- 155 ,(2000) , 10.1038/35004020
Igor Garkavtsev, Irina A. Grigorian, Valeria S. Ossovskaya, Mikhail V. Chernov, Peter M. Chumakov, Andrei V. Gudkov, The candidate tumour suppressor p33ING1 cooperates with p53 in cell growth control Nature. ,vol. 391, pp. 295- 298 ,(1998) , 10.1038/34675
Bert Vogelstein, David Lane, Arnold J. Levine, Surfing the p53 network Nature. ,vol. 408, pp. 307- 310 ,(2000) , 10.1038/35042675