ArticleOncogene2002
Tbx3 impinges on the p53 pathway to suppress apoptosis, facilitate cell transformation and block myogenic differentiation.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 102 citations in OpenAlex.
- MYC contributes to targeted therapy resistance in lung cancers driven by MET exon 14-skipping alteration.NPJ precision oncology · 2026Article
- Reduced ZMPSTE24 expression leads to prelamin accumulation and development of steatosis in MASLD patients.Scientific reports · 2025Article
- GATA6 and TBX3 gene expressions analysis of indirect inguinal hernia sacs in children.Pediatric surgery international · 2025Article
- Posttranscriptional regulation of the T-box gene midline via the 3'UTR in Drosophila is complex and cell- and tissue-dependent.Genetics · 2024Article
- The clinical and molecular characteristics of progressive hypothalamic/optic pathway pilocytic astrocytoma.Neuro-oncology · 2023Article
- Role of T-box transcription factor 3 in gastric cancers.World journal of gastrointestinal pathophysiology · 2023Review
- Cobalt-induced oxidative stress contributes to alveolar/bronchiolar carcinogenesis in B6C3F1/N mice.Archives of toxicology · 2021Article
- The c-Myc/TBX3 Axis Promotes Cellular Transformation of Sarcoma-Initiating Cells.Frontiers in oncology · 2021Article
- Review
- TBX3 knockdown suppresses the proliferation of hypopharyngeal carcinoma FaDu cells by inducing G1/S cell cycle arrest and apoptosis.Oncology letters · 2020Article
- The oncoprotein TBX3 is controlling severity in experimental arthritis.Arthritis research & therapy · 2019Article
- The transcriptional regulator TBX3 promotes progression from non-invasive to invasive breast cancer.BMC cancer · 2016Article
- TBX2 represses PTEN in rhabdomyosarcoma and skeletal muscle.Oncogene · 2016Article
- The T-box transcription factor 3 is a promising biomarker and a key regulator of the oncogenic phenotype of a diverse range of sarcoma subtypes.Oncogenesis · 2016Article
- The T-box transcription factor TBX3 drives proliferation by direct repression of the p21(WAF1) cyclin-dependent kinase inhibitor.Cell division · 2016Article
- New insights into signalling-pathway alterations in rhabdomyosarcoma.British journal of cancer · 2015Review
- Putative Breast Cancer Driver Mutations in TBX3 Cause Impaired Transcriptional Repression.Frontiers in oncology · 2015Article
- Article
- TBX2 blocks myogenesis and promotes proliferation in rhabdomyosarcoma cells.International journal of cancer · 2014Article
- Unique expression patterns of multiple key genes associated with the evolution of mammalian flight.Proceedings. Biological sciences · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tbx3 is a member of the T-box family of transcription factors. Mutations in Tbx3 cause ulnar-mammary syndrome, an autosomal dominant disorder characterized by upper limb defects, apocrine-gland defects including mammary hypoplasia, and tooth, hair and genital defects. In cell culture, Tbx3 and its close relative Tbx2 are capable of immortalizing mouse embryo fibroblasts. We show that expression of Tbx3 together with Myc or oncogenic Ras (H-Ras(Val17)) leads to efficient transformation of mouse embryo fibroblasts. Oncogene cooperation by Tbx3 correlates with an ability of Tbx3 to suppress the induction of p19ARF and p53 that is typically caused by overexpression Myc and Ras, and to protect against Myc-induced apoptosis. Whereas Tbx3 is capable of interfering with apoptosis caused by excessive Myc levels, a Tbx3 mutant lacking its C-terminal repression domain shows no anti-apoptotic activity and fails to repress levels of p19ARF or p53. Consistent with an ability to suppress p53 pathway function, we find that Tbx3, but not a Tbx3 C-terminal mutant, efficiently blocks myogenic differentiation of C2C12 myoblasts. Our results support the idea that deregulation and/or excessive levels of Tbx3 may have oncogenic potential in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.