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Stress-specific signatures: expression profiling of p53 wild-type and -null human cells

Oncogene volume 24, pages 4572–4579 (2005)Cite this article

Abstract

Gene expression responses of human cell lines exposed to a diverse set of stress agents were compared by cDNA microarray hybridization. The B-lymphoblastoid cell line TK6 (p53 wild-type) and its p53-null derivative, NH32, were treated in parallel to facilitate investigation of p53-dependent responses. RNA was extracted 4 h after the beginning of treatment when no notable decrease in cell viability was evident in the cultures. Gene expression signatures were defined that discriminated between four broad general mechanisms of stress agents: Non-DNA-damaging stresses (heat shock, osmotic shock, and 12-O-tetradecanoylphorbol 13-acetate), agents causing mainly oxidative stress (arsenite and hydrogen peroxide), ionizing radiations (neutron and γ-ray exposures), and other DNA-damaging agents (ultraviolet radiation, methyl methanesulfonate, adriamycin, camptothecin, and cis-Platinum(II)diammine dichloride (cisplatin)). Within this data set, non-DNA-damaging stresses could be discriminated from all DNA-damaging stresses, and profiles for individual agents were also defined. While DNA-damaging stresses showed a strong p53-dependent element in their responses, no discernible p53-dependent responses were triggered by the non-DNA-damaging stresses. A set of 16 genes did exhibit a robust p53-dependent pattern of induction in response to all nine DNA-damaging agents, however.

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Acknowledgements

We are grateful to S Marino and G Randers-Pehrson for operation of the Radiological Research Accelerator Facility (RARAF) van de Graaff. RARAF is an NIH supported Resource Center through Grants EB-002033 (NIBIB) and CA-37967 (NCI). We thank the Division of Computational Bioscience of the Center for Information Technology at the National Institutes of Health for providing computational resources for this study. Support from the DOE Low Dose Radiation Program, ER 63308, is gratefully acknowledged.

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Author notes

  1. Sally A Amundson

    Present address: Center for Radiological Research, Columbia University Medical Center, New York, NY, 10032, USA

  2. Michael L Bittner & Jeffrey M Trent

    Present address: Translational Genomics Research Institute (TGen), Phoenix, AZ, 85004, USA

Authors and Affiliations

  1. Gene Response Section, Center for Cancer Research, NCI, Bethesda, MD, 20892, USA

    Sally A Amundson, Khanh T Do, Lisa Vinikoor, Christine A Koch-Paiz & Albert J Fornace Jr

  2. Cancer Genetics Branch, NHGRI, Bethesda, MD, 20892, USA

    Michael L Bittner, Jeffrey M Trent & Paul Meltzer

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  1. Sally A Amundson
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  2. Khanh T Do
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Correspondence to Albert J Fornace Jr.

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Supplementary Information accompanies the paper on Oncogene website (http://www.nature.com/onc)

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Amundson, S., Do, K., Vinikoor, L. et al. Stress-specific signatures: expression profiling of p53 wild-type and -null human cells. Oncogene 24, 4572–4579 (2005). https://doi.org/10.1038/sj.onc.1208653

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