The Anti-proliferative Function of the TGF-β1 Signaling Pathway Involves the Repression of the Oncogenic TBX2 by Its Homologue TBX3
Open accessAbstract
A growing body of work has shown that the highly homologous T-box transcription factors TBX2 and TBX3 play critical but distinct roles in embryonic development and cancer progression. For example, TBX2 and TBX3 are up-regulated in several cancers and recent evidence suggests that whereas TBX2 functions as a pro-proliferative factor, TBX3 inhibits cell proliferation but promotes cancer cell migration and invasion. While the molecular mechanisms regulating these functions of TBX2 and TBX3 are poorly understood we recently reported that the TGF-β1 signaling pathway up-regulates TBX3 expression to mediate, in part, its well described anti-proliferative and pro-migratory roles. The TBX3 targets responsible for these functions were however not identified. Here we reveal for the first time that the TGF-β1 signaling pathway represses TBX2 transcriptionally and we provide a detailed mechanism to show that this is mediated by TBX3. Furthermore, we implicate the down-regulation of TBX2 in the anti-proliferative function of the TGF-β1-TBX3 axis. These findings have important implications for our understanding of the regulation of TBX2 and TBX3 and shed light on the mechanisms involved in the anti-proliferative and pro-migratory roles of TGF-β1.
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Although TBX3 promotes migration and invasiveness of cancer cells, it negatively regulates cell proliferation.
“More recently, it was recognized that although TBX3 promotes migration and invasiveness of cancer cells, it negatively regulates cell proliferation [37, 63].”
From The oncoprotein TBX3 is controlling severity in experimental arthritis (2019) · cites this paper as [63]
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- Authors
- Li, J., Ballim, D., Rodriguez, M., Cui, R., Goding, C. R., Teng, H., & Prince, S.
- Affiliations
- University of Cape Town (ZA)
- Boston University (US)
- University of Oxford (GB)
- Corresponding author
- Prince, Sharon
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2014-12
- Volume
- 289
- Issue
- 51
- Pages
- 35633-35643
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC4271245
- OpenAlex
- W1990998396
- Cited by
- 44
- References
- 39
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 7 · 2022: 1 · 2021: 2 · 2020: 3 · 2019: 4 · 2018: 5 · 2017: 5 · 2016: 4 · 2015: 4
- FWCI
- 1.78
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Research Foundation
- Cancer Association of South Africa
- University of Cape Town
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Keywords
- TGF-β1 signaling, TBX2, TBX3, T-box transcription factor, transcriptional repression, cell proliferation, tumor cell migration, tumor invasion, oncogenic transcription factor, transcriptional regulation
- MeSH terms
- Animals, Binding Sites, Cell Line, Humans, Mutation, Promoter Regions, Genetic, Protein Binding, Blotting, Western, Signal Transduction, Oncogene Proteins, Down-Regulation, Gene Expression, Reverse Transcriptase Polymerase Chain Reaction, T-Box Domain Proteins, RNA Interference, Cell Line, Tumor, Cell Proliferation, Transforming Growth Factor beta1
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