Abstract
p73, a potential tumor suppressor, is a p53 homologue. Transient over expression of p73 in cells can induce apoptosis and p21, a cellular p53 target gene primarily responsible for p53-dependent cell cycle arrest. To further characterize the role of p73 in tumor suppression, we established several groups of cell lines that inducibly express p73 under a tetracycline- regulated promoter. By using these cell lines, we found that p73 can induce both cell cycle arrest and apoptosis. We also found that p73 can activate some but not all of the previously identified p53 cellular target genes. Furthermore, we found that the transcriptional activities of p53, p73α, and p73β to induce their common cellular target genes differ among one another. These results suggest that p73 is both similar to and different from p53 in their signaling pathways leading to tumor suppression.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 5061-5065 |
| Number of pages | 5 |
| Journal | Cancer Research |
| Volume | 58 |
| Issue number | 22 |
| State | Published - Nov 15 1998 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Cancer Research
- Oncology
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The potential tumor suppressor p73 differentially regulates cellular p53 target genes. / Zhu, Jianhui; Jiang, Jieyuan; Zhou, Wenjing; Chen, Xinbin.
In: Cancer Research, Vol. 58, No. 22, 15.11.1998, p. 5061-5065.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The potential tumor suppressor p73 differentially regulates cellular p53 target genes
AU - Zhu, Jianhui
AU - Jiang, Jieyuan
AU - Zhou, Wenjing
AU - Chen, Xinbin
PY - 1998/11/15
Y1 - 1998/11/15
N2 - p73, a potential tumor suppressor, is a p53 homologue. Transient over expression of p73 in cells can induce apoptosis and p21, a cellular p53 target gene primarily responsible for p53-dependent cell cycle arrest. To further characterize the role of p73 in tumor suppression, we established several groups of cell lines that inducibly express p73 under a tetracycline- regulated promoter. By using these cell lines, we found that p73 can induce both cell cycle arrest and apoptosis. We also found that p73 can activate some but not all of the previously identified p53 cellular target genes. Furthermore, we found that the transcriptional activities of p53, p73α, and p73β to induce their common cellular target genes differ among one another. These results suggest that p73 is both similar to and different from p53 in their signaling pathways leading to tumor suppression.
AB - p73, a potential tumor suppressor, is a p53 homologue. Transient over expression of p73 in cells can induce apoptosis and p21, a cellular p53 target gene primarily responsible for p53-dependent cell cycle arrest. To further characterize the role of p73 in tumor suppression, we established several groups of cell lines that inducibly express p73 under a tetracycline- regulated promoter. By using these cell lines, we found that p73 can induce both cell cycle arrest and apoptosis. We also found that p73 can activate some but not all of the previously identified p53 cellular target genes. Furthermore, we found that the transcriptional activities of p53, p73α, and p73β to induce their common cellular target genes differ among one another. These results suggest that p73 is both similar to and different from p53 in their signaling pathways leading to tumor suppression.
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UR - http://www.scopus.com/inward/citedby.url?scp=0032533514&partnerID=8YFLogxK
M3 - Article
C2 - 9823311
AN - SCOPUS:0032533514
VL - 58
SP - 5061
EP - 5065
JO - Journal of Cancer Research
JF - Journal of Cancer Research
SN - 0099-7013
IS - 22
ER -