The T-box transcription factor, TBX3, is sufficient to promote melanoma formation and invasion
dc.contributor.author | Peres, Jade | en_ZA |
dc.contributor.author | Prince, Sharon | en_ZA |
dc.date.accessioned | 2015-11-27T09:32:39Z | |
dc.date.available | 2015-11-27T09:32:39Z | |
dc.date.issued | 2013 | en_ZA |
dc.description.abstract | The T-box transcription factor, TBX3, is overexpressed in several cancers and has been proposed as a chemotherapeutic target. Several lines of evidence suggest that TBX3 may be a key contributor to malignant melanoma, a highly aggressive and intractable disease. Using in vitro and in vivo assays we demonstrate here for the first time that overexpressing TBX3 in non-tumourigenic early stage melanoma cells is sufficient to promote tumour formation and invasion. Furthermore, we show that TBX3 may play an important role as a reciprocal switch between substrate dependent cell proliferation and tumour invasion. | en_ZA |
dc.identifier.apacitation | Peres, J., & Prince, S. (2013). The T-box transcription factor, TBX3, is sufficient to promote melanoma formation and invasion. <i>Molecular Cancer</i>, http://hdl.handle.net/11427/15392 | en_ZA |
dc.identifier.chicagocitation | Peres, Jade, and Sharon Prince "The T-box transcription factor, TBX3, is sufficient to promote melanoma formation and invasion." <i>Molecular Cancer</i> (2013) http://hdl.handle.net/11427/15392 | en_ZA |
dc.identifier.citation | Peres, J., & Prince, S. (2013). The T-box transcription factor, TBX3, is sufficient to promote melanoma formation and invasion. Mol Cancer, 12(1), 117-4598. | en_ZA |
dc.identifier.ris | TY - Journal Article AU - Peres, Jade AU - Prince, Sharon AB - The T-box transcription factor, TBX3, is overexpressed in several cancers and has been proposed as a chemotherapeutic target. Several lines of evidence suggest that TBX3 may be a key contributor to malignant melanoma, a highly aggressive and intractable disease. Using in vitro and in vivo assays we demonstrate here for the first time that overexpressing TBX3 in non-tumourigenic early stage melanoma cells is sufficient to promote tumour formation and invasion. Furthermore, we show that TBX3 may play an important role as a reciprocal switch between substrate dependent cell proliferation and tumour invasion. DA - 2013 DB - OpenUCT DO - 10.1186/1476-4598-12-117 DP - University of Cape Town J1 - Molecular Cancer LK - https://open.uct.ac.za PB - University of Cape Town PY - 2013 T1 - The T-box transcription factor, TBX3, is sufficient to promote melanoma formation and invasion TI - The T-box transcription factor, TBX3, is sufficient to promote melanoma formation and invasion UR - http://hdl.handle.net/11427/15392 ER - | en_ZA |
dc.identifier.uri | http://hdl.handle.net/11427/15392 | |
dc.identifier.uri | http://dx.doi.org/10.1186/1476-4598-12-117 | |
dc.identifier.vancouvercitation | Peres J, Prince S. The T-box transcription factor, TBX3, is sufficient to promote melanoma formation and invasion. Molecular Cancer. 2013; http://hdl.handle.net/11427/15392. | en_ZA |
dc.language.iso | eng | en_ZA |
dc.publisher | BioMed Central Ltd | en_ZA |
dc.publisher.department | Department of Human Biology | en_ZA |
dc.publisher.faculty | Faculty of Health Sciences | en_ZA |
dc.publisher.institution | University of Cape Town | |
dc.rights | This is an Open Access article distributed under the terms of the Creative Commons Attribution License | en_ZA |
dc.rights.holder | Peres and Prince; licensee BioMed Central Ltd. 2013 | en_ZA |
dc.rights.uri | http://creativecommons.org/licenses/by/2.0 | en_ZA |
dc.source | Molecular Cancer | en_ZA |
dc.source.uri | http://molecular-cancer.biomedcentral.com/ | en_ZA |
dc.subject.other | TBX3 | en_ZA |
dc.subject.other | Melanoma | en_ZA |
dc.subject.other | Migration | en_ZA |
dc.subject.other | Invasion | en_ZA |
dc.title | The T-box transcription factor, TBX3, is sufficient to promote melanoma formation and invasion | en_ZA |
dc.type | Journal Article | en_ZA |
uct.type.filetype | Text | |
uct.type.filetype | Image | |
uct.type.publication | Research | en_ZA |
uct.type.resource | Article | en_ZA |
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