The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Role of Stat3 in Regulating p53 Expression and Function
Open accessAbstract
Loss of p53 function by mutation is common in cancer. However, most natural p53 mutations occur at a late stage in tumor development, and many clinically detectable cancers have reduced p53 expression but no p53 mutations. It remains to be fully determined what mechanisms disable p53 during malignant initiation and in cancers without mutations that directly affect p53. We show here that oncogenic signaling pathways inhibit the p53 gene transcription rate through a mechanism involving Stat3, which binds to the p53 promoter in vitro and in vivo. Site-specific mutation of a Stat3 DNA-binding site in the p53 promoter partially abrogates Stat3-induced inhibition. Stat3 activity also influences p53 response genes and affects UV-induced cell growth arrest in normal cells. Furthermore, blocking Stat3 in cancer cells up-regulates expression of p53, leading to p53-mediated tumor cell apoptosis. As a point of convergence for many oncogenic signaling pathways, Stat3 is constitutively activated at high frequency in a wide diversity of cancers and is a promising molecular target for cancer therapy. Thus, repression of p53 expression by Stat3 is likely to have an important role in development of tumors, and targeting Stat3 represents a novel therapeutic approach for p53 reactivation in many cancers lacking p53 mutations.
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Cites
Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607 · cited 2×
“In particular, Stat3 signaling is usually proproliferative and antiapoptiotic (50), whereas wild-type p53 is typically antiproliferative and proapoptotic (35, 44 ).”
BackgroundDarnell, J. E., Kerr, L. M., & Stark, G. R. (1994) · Science · doi:10.1126/science.8197455 · Cited by 6,080 · cited 2×
“As a point of convergence for many growth and cytokine signaling pathways (13, 41) that are commonly overactive in tumor cells, Stat3 is constitutively activated with high frequency in diverse cancers (4, 12, 50), suggesting that repression of p53 expression by Stat3 is also likely to have a role in tumor development.”
BackgroundSTATs: transcriptional control and biological impact
Levy, D. E., & Darnell, J. E. (2002) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm909 · Cited by 3,201
The STATs of cancer — new molecular targets come of age
Yu, H., & Jove, R. (2004) · Nature Reviews Cancer · doi:10.1038/nrc1275 · Cited by 2,278
Self-citationTumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame Product p19
Kamijo, T., Zindy, F., Roussel, M. F., Quelle, D. E., Downing, J. R., Ashmun, R. A., Grosveld, G., & Sherr, C. J. (1997) · Cell · doi:10.1016/s0092-8674(00)80452-3 · Cited by 1,566
Constitutive Stat3 activity up-regulates VEGF expression and tumor angiogenesis
Niu, G., Wright, K. L., Huang, M., Song, L., Haura, E., Turkson, J., Zhang, S., Wang, T., Sinibaldi, D., Coppola, D., et al. (2002) · Oncogene · doi:10.1038/sj.onc.1205260 · Cited by 1,207
Self-citationThe role of STATs in transcriptional control and their impact on cellular function
Bromberg, J., & Darnell, J. E. (2000) · Oncogene · doi:10.1038/sj.onc.1203476 · Cited by 1,201
Transcription factors as targets for cancer therapy
Darnell, J. E. (2002) · Nature Reviews Cancer · doi:10.1038/nrc906 · Cited by 1,194
Enhanced DNA-Binding Activity of a Stat3-Related Protein in Cells Transformed by the Src Oncoprotein
Yu, C.-L., Meyer, D. J., Campbell, G. S., Larner, A. C., Carter-Su, C., Schwartz, J., & Jove, R. (1995) · Science · doi:10.1126/science.7541555 · Cited by 931
Self-citationWild-type p53 activates transcription in vitro
Farmer, G., Bargonetti, J., Zhu, H., Friedman, P., Prywes, R., & Prives, C. (1992) · Nature · doi:10.1038/358083a0 · Cited by 579 · cited 1×
“Indeed, it has been shown that the oncogenic potential of simian virus 40 (SV40) large T antigen depends on its ability to negatively regulate p53 activity, providing a mechanism by which oncoproteins inhibit p53 function in the absence of p53 mutations (3, 16, 34, 38).”
Background
Cited by
Dangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer
Grivennikov, S. I., & Karin, M. (2010) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2009.11.005 · Cited by 1,160
Yang, J., Liao, X., Agarwal, M. K., Barnes, L., Auron, P. E., & Stark, G. R. (2007) · Genes & Development · doi:10.1101/gad.1553707 · Cited by 611
STAT3 Target Genes Relevant to Human Cancers
Carpenter, R., & Lo, H.-W. (2014) · Cancers · doi:10.3390/cancers6020897 · Cited by 511
The potential and controversy of targeting STAT family members in cancer
Verhoeven, Y., Tilborghs, S., Jacobs, J., De Waele, J., Quatannens, D., Deben, C., Prenen, H., Pauwels, P., Trinh, X. B., Wouters, A., et al. (2020) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2019.10.002 · Cited by 409
Resveratrol: Its Biologic Targets and Functional Activity
Pervaiz, S., & Holme, A. L. (2009) · Antioxidants & Redox Signaling · doi:10.1089/ars.2008.2412 · Cited by 405
Metadata
- Authors
- Niu, G., Wright, K. L., Ma, Y., Wright, G. M., Huang, M., Irby, R., Briggs, J., Karras, J., Cress, W. D., Pardoll, D., Jove, R., Chen, J., & Yu, H.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2005-09-01
- Volume
- 25
- Issue
- 17
- Pages
- 7432-7440
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W2114445658
- Cited by
- 392
- References
- 10
- FWCI
- 5.37
- Type
- journal article
- Language
- en
- Open access
- green
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- Niu, G., Wright, K. L., Ma, Y., Wright, G. M., Huang, M., Irby, R., Briggs, J., Karras, J., Cress, W. D., Pardoll, D., Jove, R., Chen, J., & Yu, H. (2005). Role of Stat3 in Regulating p53 Expression and Function. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.25.17.7432-7440.2005
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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