The T-box transcription factor TBX3 drives proliferation by direct repression of the p21WAF1 cyclin-dependent kinase inhibitor

dc.contributor.authorWillmer, Tarryn
dc.contributor.authorHare, Shannagh
dc.contributor.authorPeres, Jade
dc.contributor.authorPrince, Sharon
dc.date.accessioned2016-05-23T06:55:28Z
dc.date.available2016-05-23T06:55:28Z
dc.date.issued2016-04-22
dc.date.updated2016-05-19T09:29:04Z
dc.description.abstractBackground: TBX3, a member of the T-box family of transcription factors, is essential in development and has emerged as an important player in the oncogenic process. TBX3 is overexpressed in several cancers and has been shown to contribute directly to tumour formation, migration and invasion. However, little is known about the molecular basis for its role in development and oncogenesis because there is a paucity of information regarding its target genes. The cyclin-dependent kinase inhibitor p21WAF1 plays a pivotal role in a myriad of processes including cell cycle arrest, senescence and apoptosis and here we provide a detailed mechanism to show that it is a direct and biologically relevant target of TBX3. Results: Using a combination of luciferase reporter gene assays and in vitro and in vivo binding assays we show that TBX3 directly represses the p21WAF1 promoter by binding a T-element close to its initiator. Furthermore, we show that the TBX3 DNA binding domain is required for the transcriptional repression of p21WAF1 and that pseudo-phosphorylation of a serine proline motif (S190) located within this domain may play an important role in regulating this ability. Importantly, we demonstrate using knockdown and overexpression experiments that p21WAF1 repression by TBX3 is biologically significant and required for TBX3-induced cell proliferation of chondrosarcoma cells. Conclusions: Results from this study provide a detailed mechanism of how TBX3 transcriptionally represses p21WAF1 which adds to our understanding of how it may contribute to oncogenesis.en_ZA
dc.identifier.apacitationWillmer, T., Hare, S., Peres, J., & Prince, S. (2016). The T-box transcription factor TBX3 drives proliferation by direct repression of the p21WAF1 cyclin-dependent kinase inhibitor. <i>Cell Division</i>, http://hdl.handle.net/11427/19767en_ZA
dc.identifier.chicagocitationWillmer, Tarryn, Shannagh Hare, Jade Peres, and Sharon Prince "The T-box transcription factor TBX3 drives proliferation by direct repression of the p21WAF1 cyclin-dependent kinase inhibitor." <i>Cell Division</i> (2016) http://hdl.handle.net/11427/19767en_ZA
dc.identifier.citationWillmer, T., Hare, S., Peres, J., & Prince, S. (2016). The T-box transcription factor TBX3 drives proliferation by direct repression of the p21 WAF1 cyclin-dependent kinase inhibitor. Cell Division, 11(1), 1.en_ZA
dc.identifier.issn1747-1028en_ZA
dc.identifier.ris TY - Journal Article AU - Willmer, Tarryn AU - Hare, Shannagh AU - Peres, Jade AU - Prince, Sharon AB - Background: TBX3, a member of the T-box family of transcription factors, is essential in development and has emerged as an important player in the oncogenic process. TBX3 is overexpressed in several cancers and has been shown to contribute directly to tumour formation, migration and invasion. However, little is known about the molecular basis for its role in development and oncogenesis because there is a paucity of information regarding its target genes. The cyclin-dependent kinase inhibitor p21WAF1 plays a pivotal role in a myriad of processes including cell cycle arrest, senescence and apoptosis and here we provide a detailed mechanism to show that it is a direct and biologically relevant target of TBX3. Results: Using a combination of luciferase reporter gene assays and in vitro and in vivo binding assays we show that TBX3 directly represses the p21WAF1 promoter by binding a T-element close to its initiator. Furthermore, we show that the TBX3 DNA binding domain is required for the transcriptional repression of p21WAF1 and that pseudo-phosphorylation of a serine proline motif (S190) located within this domain may play an important role in regulating this ability. Importantly, we demonstrate using knockdown and overexpression experiments that p21WAF1 repression by TBX3 is biologically significant and required for TBX3-induced cell proliferation of chondrosarcoma cells. Conclusions: Results from this study provide a detailed mechanism of how TBX3 transcriptionally represses p21WAF1 which adds to our understanding of how it may contribute to oncogenesis. DA - 2016-04-22 DB - OpenUCT DO - 10.1186/s13008-016-0019-0 DP - University of Cape Town J1 - Cell Division KW - Transcription factor KW - p21WAF1 KW - Cancer LK - https://open.uct.ac.za PB - University of Cape Town PY - 2016 SM - 1747-1028 T1 - The T-box transcription factor TBX3 drives proliferation by direct repression of the p21WAF1 cyclin-dependent kinase inhibitor TI - The T-box transcription factor TBX3 drives proliferation by direct repression of the p21WAF1 cyclin-dependent kinase inhibitor UR - http://hdl.handle.net/11427/19767 ER - en_ZA
dc.identifier.urihttp://dx.doi.org/10.1186/s13008-016-0019-0
dc.identifier.urihttp://hdl.handle.net/11427/19767
dc.identifier.vancouvercitationWillmer T, Hare S, Peres J, Prince S. The T-box transcription factor TBX3 drives proliferation by direct repression of the p21WAF1 cyclin-dependent kinase inhibitor. Cell Division. 2016; http://hdl.handle.net/11427/19767.en_ZA
dc.languageengen_ZA
dc.language.rfc3066en
dc.publisherBioMed Centralen_ZA
dc.publisher.departmentDepartment of Human Biologyen_ZA
dc.publisher.facultyFaculty of Health Sciencesen_ZA
dc.publisher.institutionUniversity of Cape Town
dc.rightsCreative Commons Attribution 4.0 International (CC BY 4.0)*
dc.rights.holderWillmer et al.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_ZA
dc.sourceCell Divisionen_ZA
dc.source.urihttp://celldiv.biomedcentral.com/
dc.subjectTranscription factor
dc.subjectp21WAF1
dc.subjectCancer
dc.titleThe T-box transcription factor TBX3 drives proliferation by direct repression of the p21WAF1 cyclin-dependent kinase inhibitoren_ZA
dc.typeJournal Articleen_ZA
uct.type.filetypeText
uct.type.filetypeImage
uct.type.publicationResearchen_ZA
uct.type.resourceArticleen_ZA
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