Stat3 as an Oncogene
Open accessAbstract
STATs are latent transcription factors that mediate cytokine- and growth factor-directed transcription. In many human cancers and transformed cell lines, Stat3 is persistently activated, and in cell culture, active Stat3 is either required for transformation, enhances transformation, or blocks apoptosis. We report that substitution of two cysteine residues within the C-terminal loop of the SH2 domain of Stat3 produces a molecule that dimerizes spontaneously, binds to DNA, and activates transcription. The Stat3-C molecule in immortalized fibroblasts causes cellular transformation scored by colony formation in soft agar and tumor formation in nude mice. Thus, the activated Stat3 molecule by itself can mediate cellular transformation and the experiments focus attention on the importance of constitutive Stat3 activation in human tumors.
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A constitutively active form of STAT3 causes cellular transformation in immobilized fibroblasts.
“Furthermore, a constitutively active form of STAT3 causes cellular transformation in immobilized fibroblasts (26”
From STAT3 Contributes to the Mitogenic Response of Hepatocytes during Liver Regeneration (2002) · cites this paper as [26]
STAT3 transcriptionally activates genes of several anti-autophagy-related proteins e.g., BCL2, BCL2L1, and MCL1.
“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 Bromberg et al., 1999
Hyperactivation of STAT3 is a salient attribute of many cancers.
“Hyperactivation of STAT3 is a salient attribute of many cancers”
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 Bromberg et al., 1999
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- Authors
- Bromberg, J. F., Wrzeszczynska, M. H., Devgan, G., Zhao, Y., Pestell, R. G., Albanese, C., & Darnell, J. E.
- Affiliations
- Rockefeller University (US)
- Albert Einstein College of Medicine (US)
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1999-08
- Volume
- 98
- Issue
- 3
- Pages
- 295-303
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2074356752
- Cited by
- 2,790
- References
- 3
- Citations by year
- 2026: 28 · 2025: 33 · 2024: 55 · 2023: 63 · 2022: 64 · 2021: 83 · 2020: 81 · 2019: 88 · 2018: 78 · 2017: 126 · 2016: 111 · 2015: 130 · 2014: 145 · 2013: 173 · 2012: 150
- FWCI
- 37.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (R29-CA-70897, R01CA075503)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- STAT3, oncogenes, constitutive STAT3 activation, protein dimerization, transcriptional activation, cell transformation, apoptosis resistance, cytokine signaling, fibroblasts, tumor formation
- MeSH terms
- Acute-Phase Proteins, Animals, Cell Line, Cell Transformation, Neoplastic, DNA-Binding Proteins, Gene Expression Regulation, Humans, Mice, Nude, Neoplasms, Experimental, Oncogenes, Recombinant Fusion Proteins, Transcription, Genetic, Transfection, Tumor Cells, Cultured, Trans-Activators, 3T3 Cells, src Homology Domains, Amino Acid Substitution, STAT3 Transcription Factor, Mice
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