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STATs in oncogenesis
Abstract
Since their discovery as key mediators of cytokine signaling, considerable progress has been made in defining the structure-function relationships of Signal Transducers and Activators of Transcription (STATs). In addition to their central roles in normal cell signaling, recent studies have demonstrated that diverse oncoproteins can activate specific STATs (particularly Stat3 and Stat5) and that constitutively-activated STAT signaling directly contributes to oncogenesis. Furthermore, extensive surveys of primary tumors and cell lines derived from tumors indicate that inappropriate activation of specific STATs occurs with surprisingly high frequency in a wide variety of human cancers. Together, these findings provide compelling evidence that aberrant STAT activation associated with oncogenesis is not merely adventitious but instead contributes to the process of malignant transformation. These studies are beginning to reveal the molecular mechanisms leading to STAT activation in the context of oncogenesis, and candidate genes regulated by STATs that may contribute to oncogenesis are being identified. Recent studies suggest that activated STAT signaling participates in oncogenesis by stimulating cell proliferation and preventing apoptosis. This review presents the evidence for critical roles of STATs in oncogenesis and discusses the potential for development of novel cancer therapies based on mechanistic understanding of STAT signaling. Oncogene (2000).
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“STAT3 transcriptionally activates genes of several anti-autophagy–related proteins e.g., BCL2, BCL2L1, and MCL1 (Fukada et al., 1996; Bromberg et al., 1999; Bowman et al., 2000).”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Bowman et al., 2000
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“Sorafenib, a small-molecule kinase insert domain receptor inhibitor, activates autophagy in multiple liver cancer cell lines through targeting STAT3 and reducing MCL1 expression (Tai et al., 2013).”
BackgroundChemotherapy-enhanced inflammation may lead to the failure of therapy and metastasis
Vyas, D., Laput, G. P., & Vyas, A. K. (2014) · OncoTargets and Therapy · doi:10.2147/ott.s60114 · Cited by 316
Reich, N. C., & Liu, L. (2006) · Nature Reviews Immunology · doi:10.1038/nri1885 · Cited by 376
RNA Viruses: ROS-Mediated Cell Death
Reshi, L., Su, Y.-C., & Hong, J. (2014) · International Journal of Cell Biology · doi:10.1155/2014/467452 · Cited by 314
Integration of EGFR inhibitors with radiochemotherapy
Nyati, M. K., Morgan, M. A., Feng, F. Y.-C., & Lawrence, T. S. (2006) · Nature reviews. Cancer · doi:10.1038/nrc1953 · Cited by 302
Nuclear Receptor Coregulators and Human Disease
Lonard, D. M., Lanz, R. B., & O’Malley, B. W. (2007) · Endocrine Reviews · doi:10.1210/er.2007-0012 · Cited by 318
Kanda, N., Seno, H., Konda, Y., Marusawa, H., Kanai, M., Nakajima, T., Kawashima, T., Nanakin, A., Sawabu, T., Uenoyama, Y., et al. (2004) · Oncogene · doi:10.1038/sj.onc.1207606 · Cited by 305
Pfeffer, S. R., Yang, C. H., & Pfeffer, L. M. (2015) · Drug Development Research · doi:10.1002/ddr.21257 · Cited by 325
Ding, B. B., Yu, J., Yu, R. Y.-L., Mendez, L., Shaknovich, R., Zhang, Y., Cattoretti, G., & Ye, B. H. (2007) · Blood · doi:10.1182/blood-2007-04-087734 · Cited by 301
Indirubin derivatives inhibit Stat3 signaling and induce apoptosis in human cancer cells
Nam, S., Buettner, R., Turkson, J., Kim, D., Cheng, J. Q., Muehlbeyer, S., Hippe, F., Vatter, S., Merz, K., Eisenbrand, G., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0409467102 · Cited by 297
Self-citationSTAT proteins as novel targets for cancer drug discovery
Turkson, J. (2004) · Expert Opinion on Therapeutic Targets · doi:10.1517/14728222.8.5.409 · Cited by 297
Self-citationSTAT‐mediated EGFR signaling in cancer
Quesnelle, K. M., Boehm, A. L., & Grandis, J. R. (2007) · Journal of Cellular Biochemistry · doi:10.1002/jcb.21475 · Cited by 300
Bhattacharya, S., Ray, R. M., & Johnson, L. R. (2005) · Biochemical Journal · doi:10.1042/bj20050465 · Cited by 299
Metadata
- Authors
- Bowman, T., Garcia, R., Turkson, J., & Jove, R.
- Affiliations
- Moffitt Cancer Center (US)
- University of South Florida (US)
- ORCID
- Turkson, James
- Venue
- Oncogene
- Published
- 2000-05-25
- Volume
- 19
- Issue
- 21
- Pages
- 2474-2488
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2024282024
- Cited by
- 1,743
- References
- 152
- Citations by year
- 2026: 16 · 2025: 18 · 2024: 18 · 2023: 22 · 2022: 39 · 2021: 48 · 2020: 44 · 2019: 45 · 2018: 59 · 2017: 63 · 2016: 58 · 2015: 104 · 2014: 80 · 2013: 82 · 2012: 89
- FWCI
- 7.25
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- STAT, signal transducer and activator of transcription, carcinogenesis, STAT3, STAT5, malignant transformation, cytokine signaling, cell proliferation, apoptosis, cancer therapy targets, cancer cell lines
- MeSH terms
- Animals, Cell Transformation, Neoplastic, DNA-Binding Proteins, Humans, Neoplasms, Phosphorylation, Phosphoserine, Protein-Tyrosine Kinases, Signal Transduction, Oncogene Proteins, Trans-Activators, Gene Expression Regulation, Neoplastic, STAT1 Transcription Factor
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