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 methane-sulfonate, 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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 4572-4579 |
| Number of pages | 8 |
| Journal | Oncogene |
| Volume | 24 |
| Issue number | 28 |
| DOIs | |
| State | Published - Jun 30 2005 |
| Externally published | Yes |
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Keywords
- cDNA microarray
- DNA damage
- Heavy metals
- p53
ASJC Scopus subject areas
- Molecular Biology
- Cancer Research
- Genetics
Cite this
Stress-specific signatures : Expression profiling of p53 wild-type and -null human cells. / Amundson, Sally A.; Do, Khanh T.; Vinikoor, Lisa; Koch-Paiz, Christine A.; Bittner, Michael L.; Trent, Jeffrey M.; Meltzer, Paul; Fornace, Albert J.
In: Oncogene, Vol. 24, No. 28, 30.06.2005, p. 4572-4579.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Stress-specific signatures
T2 - Expression profiling of p53 wild-type and -null human cells
AU - Amundson, Sally A.
AU - Do, Khanh T.
AU - Vinikoor, Lisa
AU - Koch-Paiz, Christine A.
AU - Bittner, Michael L.
AU - Trent, Jeffrey M.
AU - Meltzer, Paul
AU - Fornace, Albert J.
PY - 2005/6/30
Y1 - 2005/6/30
N2 - 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 methane-sulfonate, 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.
AB - 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 methane-sulfonate, 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.
KW - cDNA microarray
KW - DNA damage
KW - Heavy metals
KW - p53
UR - http://www.scopus.com/inward/record.url?scp=21444458033&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=21444458033&partnerID=8YFLogxK
U2 - 10.1038/sj.onc.1208653
DO - 10.1038/sj.onc.1208653
M3 - Article
C2 - 15824734
AN - SCOPUS:21444458033
VL - 24
SP - 4572
EP - 4579
JO - Oncogene
JF - Oncogene
SN - 0950-9232
IS - 28
ER -