The T-box transcription factor, TBX3, is a key substrate of AKT3 in melanomagenesis
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// Jade Peres 1 , Shaheen Mowla 1 , Sharon Prince 1 1 Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Observatory, 7925, Cape Town, South Africa Correspondence to: Sharon Prince, e-mail: sharon.prince@uct.ac.za Keywords: TBX3, AKT3, melanoma, E-cadherin, T-box factors Received: September 12, 2014 Accepted: November 19, 2014 Published: December 16, 2014 ABSTRACT The AKT3 signalling pathway plays a critical role in melanoma formation and invasion and components of this signalling cascade are therefore attractive targets for the treatment of malignant melanoma. Recent evidence show that the embryonically important TBX3 transcription factor is upregulated in a subset of melanomas and plays a key role in promoting melanoma formation and invasion, in part by repressing the cell adhesion molecule E-cadherin. We have identified TBX3 as a key substrate of AKT3 in melanomagenesis. Briefly, using site-directed mutagenesis and in vitro kinase assays, we have identified the AKT3 target site at serine residue 720 in the TBX3 protein and show that this site is phosphorylated in vivo . Importantly, we show by western blotting, immunofluorescence, reporter, migration and invasion assays that the phosphorylation at S720 promotes TBX3 protein stability, nuclear localization, transcriptional repression of E-cadherin, and its role in cell migration and invasion. Our results identify a novel signalling and transcriptional network linking AKT3, TBX3 and E-cadherin during melanoma migration and invasion and reveals TBX3 as a potential target for anti-metastatic therapeutics.
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TBX3 has previously been shown to directly interact with these signaling cascades in other cell types to regulate cell survival and proliferation.
“TBX3 has previously been shown to directly interact with these signaling cascades in other cell types to regulate cell survival and proliferation [54–57]”
From The oncoprotein TBX3 is controlling severity in experimental arthritis (2019) · cites this paper as [56]
The Discussion (page unavailable) reports TBX3 interactions with PI3K/AKT signaling in mouse embryonic stem cells and with p38 MAPK in COS cells, supporting the reference to other cell types. It also describes PI3K/AKT as promoting survival and proliferation in melanoma, but does not establish that TBX3’s interactions with those cascades regulate both outcomes in other cell types. (LLM, conf=0.82)
Experimental — accuracy not yet measuredA few kinases participate in phosphorylation of TBX3, such as AKT3 at S720, cyclin A-CDK2 at either S190 or S354, p38 MAP kinase at S692, and AKT1 is also involved.
“Moreover, a few kinases participate in phosphorylation of TBX3, such as AKT3 at S720, cyclin A-CDK2 at either S190 or S354, p38 MAP kinase at S692, and AKT1 is also involved54,59–61.”
From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [59]
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“Phosphorylation of TBX3 While there are several predicted post-translational modification sites for TBX3 including 10 ubiquitination, 1 acetylation, 2 methylation and 29 phosphorylation sites only the SP190, SP692 and S720 phosphorylation sites have been fully characterised.”
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Huang, L., Zhang, X., Li, F., & Wang, X. (2022) · Computational and Mathematical Methods in Medicine · doi:10.1155/2022/2880087 · Cited by 3 · see citing works
RetractedHuang, Q., Chu, X., Yang, C., Huai, Y., He, C., Ma, X., Pei, J., Gao, J., Liu, Z., Jiang, S., et al. (2025) · Cancer Cell International · doi:10.1186/s12935-025-03856-1 · Cited by 2 · see citing works
Role of T-box transcription factor 3 in gastric cancers
Asano, N., Imatani, A., Takeuchi, A., Saito, M., Jin, X., Hatta, W., Uno, K., Koike, T., & Masamune, A. (2023) · World Journal of Gastrointestinal Pathophysiology · doi:10.4291/wjgp.v14.i2.12 · Cited by 2 · see citing works
Ncube, S. M., ArulJothi, K. N., Lang, D. M., Sinkala, M., Burmeister, C. A., Serala, K., Blackburn, J. M., & Prince, S. (2024) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-23-1031 · Cited by 1 · see citing works
Self-citationSimplifying causal gene identification in GWAS loci
Schipper, M., Ulirsch, J. C., Posthuma, D., Ripke, S., & Heilbron, K. (2026) · PLoS Genetics · doi:10.1371/journal.pgen.1012079 · Cited by 1 · see citing works
Higgins, G., Higgins, F., Peres, J., Lang, D. M., Abdalrahman, T., Zaman, M. H., Prince, S., & Franz, T. (2023) · Experimental Cell Research · doi:10.1016/j.yexcr.2023.113633 · Cited by 1 · see citing works
Self-citationGenetic Profiling of Primary Versus Metastatic Ewing Sarcoma for Therapeutic Target Identification
Mitchell, C., Voskamp, S., Geagea, E., Anand, D., Nelson, J., & Lovejoy, J. (2026) · Life · doi:10.3390/life16060901
- Authors
- Peres, J., Mowla, S., & Prince, S.
- Affiliations
- University of Cape Town (ZA)
- Corresponding author
- Prince, Sharon
- Venue
- Oncotarget
- Publisher
- Impact Journals, LLC
- Published
- 2014-12-16
- Volume
- 6
- Issue
- 3
- Pages
- 1821-1833
- ISSN
- 1949-2553 (ISSN-L)
- PMC
- PMC4359334
- OpenAlex
- W2169096028
- Cited by
- 40
- References
- 51
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 6 · 2023: 3 · 2022: 3 · 2021: 1 · 2020: 3 · 2019: 5 · 2018: 3 · 2017: 4 · 2016: 6 · 2015: 1
- FWCI
- 1.50
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- cc-by
- Locations
- Oncotarget (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- 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 › Melanoma and MAPK Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- TBX3, AKT3, melanoma, melanomagenesis, E-cadherin, protein phosphorylation, protein stability, nuclear localization, transcriptional repression, cell migration, tumor invasion, Akt signaling, anti-metastatic therapy
- MeSH terms
- Humans, Melanoma, Phosphorylation, Transfection, Cadherins, Up-Regulation, Mutagenesis, Site-Directed, T-Box Domain Proteins, Proto-Oncogene Proteins c-akt
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