ArticleBMC cancer2016
The transcriptional regulator TBX3 promotes progression from non-invasive to invasive breast cancer.
Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- TBX3 shapes an immunosuppressive microenvironment and induces immunotherapy resistance.Theranostics · 2025Article
- SIRT6 promotes metastasis and relapse in HER2-positive breast cancer.Scientific reports · 2023Article
- Abnormal activation of the Wnt3a/β-catenin signaling pathway promotes the expression of T-box transcription factor 3(TBX3) and the epithelial-mesenchymal transition pathway to mediate the occurrence of adenomyosis.Molecular biology reports · 2023Article
- Wnt Signaling and Aging of the Gastrointestinal Tract.International journal of molecular sciences · 2022Review
- CREB5 reprograms FOXA1 nuclear interactions to promote resistance to androgen receptor-targeting therapies.eLife · 2022Article
- Article
- Isoform-specific promotion of breast cancer tumorigenicity by TBX3 involves induction of angiogenesis.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Review
- Classifying Breast Cancer Molecular Subtypes by Using Deep Clustering Approach.Frontiers in genetics · 2020Article
- TBX3 promotes progression of pre-invasive breast cancer cells by inducing EMT and directly up-regulating SLUG.The Journal of pathology · 2019Article
- Genetic variation in sensitivity to estrogens and breast cancer risk.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Novel HDAC5-interacting motifs of Tbx3 are essential for the suppression of E-cadherin expression and for the promotion of metastasis in hepatocellular carcinoma.Signal transduction and targeted therapyArticle
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTBX3 is a T-box transcription factor repressor that is elevated in metastatic breast cancer and is believed to promote malignancy of tumor cells, possibly by promoting cell survival and epithelial-mesenchymal transition.
methodsThe relative expression of TBX3 was assessed in the 21T cell lines which were derived from an individual patient and represent three distinct stages of breast cancer progression: 21PT, atypical ductal hyperplasia; 21NT, ductal carcinoma in situ; and 21MT-1, invasive mammary carcinoma. Two different isoforms of TBX3 (TBX3iso1 and TBX3iso2) were overexpressed to evaluate cell survival/colony forming ability, growth, and invasion in the ductal carcinoma in situ-like 21NT cell line using an in vitro Matrigel model of cancer progression. In addition, TBX3 expression was knocked down to evaluate the effects of downregulating TBX3 on the invasive mammary carcinoma-like 21MT-1 cell line. Finally, PCR array profiling was used to assess alterations in gene expression due to TBX3 overexpression in the 21NT cells.
resultsTBX3 is abundant in the invasive 21MT-1 cell line, while being minimally expressed in the non-invasive 21NT and 21PT cell lines. Overexpression of either TBX3iso1 or TBX3iso2 in 21NT cells resulted in increased cell survival/colony forming ability, growth vs. apoptosis and invasion in Matrigel. In contrast, short hairpin RNA-mediated knockdown of TBX3 in the 21MT-1 cells resulted in smaller colonies, with a more regular, less dispersed (less infiltrative) morphology. Array profiling of the 21NT TBX3 iso1 and iso2 transfectants showed that there are common alterations in expression of several genes involved in signal transduction, cell cycle control/cell survival, epithelial-mesenchymal transition and invasiveness.
conclusionsOverall, these results indicate that TBX3 (isoform 1 or 2) expression can promote progression in a model of early breast cancer by altering cell properties involved in cell survival/colony formation and invasiveness, as well as key regulatory and EMT/invasiveness-related gene expressions.
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