Stress signals induce transcriptionally inactive E2F-1 independently of p53 and Rb (original) (raw)
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- Published: 23 May 2000
Oncogene volume 19, pages 2369–2376 (2000) Cite this article
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Abstract
One of the common features of cellular response to stress is cell cycle arrest or apoptosis. E2F is one of the key factors which controls cell cycle progression. Overexpression of E2F-1 can also induce apoptosis. In order to understand the role of E2F-1 in cellular response to stress, we studied the E2F-1 response in various cell lines to different types of stress signals including UV irradiation, cisplatin, etoposide and hypoxia. We showed here that the expression level of E2F-1 can be up regulated by the treatment of DNA damage agents as well as hypoxia. The kinetics of E2F-1 increase was dependent on the types of inducer and was similar to that of p53. However, stress signals can induce E2F-1 expression independently of p53 and Rb. Furthermore, the induced E2F-1 was transcriptionally inactive. All these results suggested that E2F-1 may play a very important role in cellular response to stress and this novel role of E2F-1 is independent of its transactivation function.
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References
- Amellem Q, Stokke T, Sandvik JA and Pettersen EO . 1996 Exp Cell Res 227: 106–115
- Blattner C, Sparks A and Lane D . 1999 Mol Cell Biol 19: 3704–3713
- Chellappan SP, Hiebert S, Mudryj M, Horowitz JM and Nevins JR . 1991 Cell 65: 1053–1061
- DeGregori J, Leone G, Miron A, Jakoi L and Nevins JR . 1997 Proc Natl Acad Sci USA 94: 7245–7250
- Di Como CJ, Gaiddon C and Prives C . 1999 Mol Cell Biol 19: 1438–1449
- Field SJ, Tsai FY, Kuo F, Zubiaga AM, Kaelin JWG, Livingston DM, Orkin SH and Greenberg ME . 1996 Cell 85: 549–561
- Graeber TG, Osmanian C, Jacks T, Housman DE, Koch CJ, Lowe SW and Giaccia AJ . 1996 Nature 379: 88–91
- Graeber TG, Peterson JF, Tsai M, Monica K, Fornace JAJ and Giaccia AJ . 1994 Mol Cell Biol 14: 6264–6277
- Haas-Kogan DA, Kogan SC, Levi D, Dazin P, T'Ang A, Fung Y-KT and Israel MA . 1995 EMBO J 14: 461–472
- Hijmans EM, Voorhoeve PM, Beijersbergen RL, Van'T Veer LJ and Bernards R . 1995 Mol Cell Biol 15: 3082–3089
- Hofferer M, Wirbelauer C, Humar B and Krek W . 1999 Nucleic Acids Res 27: 491–495
- Hofmann F, Martelli F, Livingston DM and Wang Z . 1996 Genes Dev 10: 2949–2959
- Holmberg C, Helin K, Sehested M and Karlstrom O . 1998 Oncogene 17: 143–155
- Hsieh J-K, Fredersdorf S, Kauzarides T, Martin K and Lu X . 1997 Genes Dev 11: 1840–1852
- Huang Y, Ishiko T, Nakada S, Utsugisawa T, Kato T and Yuan Z-M . 1997 Cancer Res 57: 3640–3643
- Johnson DG, Cress WD, Jakoi L and Nevins JR . 1994 Proc Natl Acad Sci USA 91: 12823–12827
- Johnson DG, Schwarz JK, Cress WD and Nevins JR . 1993 Nature 365: 349–352
- Ko LJ and Prives C . 1996 Genes Dev 10: 1054–1072
- Krtolica A, Krucher N and Ludlow J . 1998 Oncogene 17: 2295–2304
- La Thangue NB . 1994 TIBS 19: 108–114
- Lam EW-F and La Thangue NB . 1994 Curr Opin Cell Biol 6: 859–866
- Lu X and Lane DP . 1993 Cell 75: 765–778
- Marti A, Wirbelauer C, Scheffner M and Krek W . 1999 Nature Cell Biology 1: 14–19
- Nip JS, Strom DK, Fee BE, Zambetti G, Clevland JL and Hiebert SW . 1997 Mol Cell Biol 17: 1049–1056
- Phillips AC, Bates S, Ryan KM, Helin K and Vousden KH . 1997 Genes Dev 11: 1853–1863
- Pierce AM, Fisher SM, Conti CJ and Johnson DG . 1998 Oncogene 16: 1267–1276
- Qin XQ, Livingston DM, Kaelin WGJ and Adams PD . 1994 Proc Natl Acad Sci USA 91: 10918–10922
- Sardet C, Vidal M, Cobrinik D, Geng Y, Onufryk C and Chen A . 1995 Proc Natl Acad Sci USA 92: 2403–2407
- Shan B and Lee WH . 1994 Mol Cell Biol 14: 8166–8173
- Singh P, Wong SH and Hong W . 1994 EMBO J 13: 3329–3338
- Trimarchi JM, Fairchild B, Verona R, Moberg K, Andon N and Lee JA . 1998 Proc Natl Acad Sci USA 95: 2850–2858
- Vandel L and Kouzarides T . 1999 EMBO J 18: 4280–4291
- Wu X and Levine AJ . 1994 Proc Natl Acad Sci USA 91: 3602–3606
- Yamasaki L, Jacks T, Bronson R, Goillot E, Harlow E and Dyson NJ . 1996 Cell 85: 537–548
- Zhang Y and Chellappan SP . 1995 Oncogene 10: 2085–2093
Acknowledgements
We would like to thank Lynn Fallis and Florence Chan for the technical help and this work was supported by the Ludwig Institue for Cancer Research.
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Authors and Affiliations
- Ludwig Institute for Cancer Research, Imperial College of Science, Technology and Medicine at St. Mary's Campus, Norfolk Place, London, W2 1PG
Daniel J O'Connor & Xin Lu
Authors
- Daniel J O'Connor
- Xin Lu
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O'Connor, D., Lu, X. Stress signals induce transcriptionally inactive E2F-1 independently of p53 and Rb.Oncogene 19, 2369–2376 (2000). https://doi.org/10.1038/sj.onc.1203540
- Received: 16 December 1999
- Revised: 22 February 2000
- Accepted: 23 February 2000
- Published: 23 May 2000
- Issue date: 11 May 2000
- DOI: https://doi.org/10.1038/sj.onc.1203540