This Article Full Text Full Text (PDF) Supplementary Data Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Untergasser, G. Articles by Hermeking, H. Search for Related Content PubMed PubMed Citation Articles by Untergasser, G. Articles by Hermeking, H.

Characterization of Epithelial Senescence by Serial Analysis of Gene Expression

Identification of Genes Potentially Involved in Prostate Cancer¹

Molecular Oncology, Max-Planck-Institute of Biochemistry, Am Klopferspitz 18 A, D-82152 Martinsried/Munich, Germany

Evasion of cellular senescence is required for the immortal phenotype of tumor cells. The tumor suppressor genes p16^INK4A, pRb, and p53 have been implicated in the induction of cellular senescence. To identify additional genes and pathways involved in the regulation of senescence in prostate epithelial cells (PrECs), we performed serial analysis of gene expression (SAGE). The gene expression pattern of human PrECs arrested because of senescence was compared with the pattern of early passage cells arrested because of confluence. A total of 144,137 SAGE tags representing 25,645 unique mRNA species was collected and analyzed: 157 mRNAs (70 with known function) were up-regulated and 116 (65 with known function) were down-regulated significantly in senescent PrECs (P < 0.05; fold difference >2.5). The differential regulation of an exemplary set of genes during senescence was confirmed by quantitative real-time PCR in PrECs derived from three different donors. The results presented here provide the molecular basis of the characteristic changes in morphology and proliferation observed in senescent PrECs. Furthermore, the differentially expressed genes identified in this report will be instrumental in the further analysis of cellular senescence in PrECs and may lead to the identification of tumor suppressor genes and proto-oncogenes involved in the development of prostate cancer.

This article has been cited by other articles:

				K. Gosselin, E. Deruy, S. Martien, C. Vercamer, F. Bouali, T. Dujardin, C. Slomianny, L. Houel-Renault, F. Chelli, Y. De Launoit, et al. Senescent Keratinocytes Die by Autophagic Programmed Cell Death Am. J. Pathol., February 1, 2009; 174(2): 423 - 435. [Abstract] [Full Text] [PDF]

				L. L. Song, F. Alimirah, R. Panchanathan, H. Xin, and D. Choubey Expression of an IFN-Inducible Cellular Senescence Gene, IFI16, Is Up-Regulated by p53 Mol. Cancer Res., November 1, 2008; 6(11): 1732 - 1741. [Abstract] [Full Text] [PDF]

				D. Lodygin, A. Epanchintsev, A. Menssen, J. Diebold, and H. Hermeking Functional Epigenomics Identifies Genes Frequently Silenced in Prostate Cancer Cancer Res., May 15, 2005; 65(10): 4218 - 4227. [Abstract] [Full Text] [PDF]

				D M Peehl Primary cell cultures as models of prostate cancer development Endocr. Relat. Cancer, March 1, 2005; 12(1): 19 - 47. [Abstract] [Full Text] [PDF]

				J. Walter-Yohrling, X. Cao, M. Callahan, W. Weber, S. Morgenbesser, S. L. Madden, C. Wang, and B. A. Teicher Identification of Genes Expressed in Malignant Cells That Promote Invasion Cancer Res., December 15, 2003; 63(24): 8939 - 8947. [Abstract] [Full Text] [PDF]