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dc.contributor.authorWake, Matthew Sen
dc.contributor.authorWatson, Christineen
dc.date.accessioned2015-05-28T09:29:38Z
dc.date.available2015-05-28T09:29:38Z
dc.date.issued2015-04-22en
dc.identifier.citationFEBS Journal Volume 282, Issue 14, pages 2600–2611, July 2015. DOI: 10.1111/febs.13285en
dc.identifier.issn1742-464X
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/248047
dc.description.abstractThe STAT family of transcription factors (signal transducers and activators of transcription) transduce signals from cytokine receptors to the nucleus, where STAT dimers bind to DNA and regulate transcription. STAT3 is the most ubiquitous of the STATs, being activated by a wide variety of cytokines and growth factors. STAT3 has many roles in physiological processes such as inflammatory signalling, aerobic glycolysis and immune suppression, and was also the first family member shown to be aberrantly activated in a wide range of both solid and liquid tumours. STAT3 promotes tumorigenesis by regulating the expression of various target genes, including cell-cycle regulators, angiogenic factors and anti-apoptosis genes. Paradoxically, in some circumstances, STAT3 signalling induces cell death. The best known example is the involuting mammary gland, where STAT3 is essential for induction of a lysosomal pathway of cell death. Nevertheless, direct silencing or inhibition of STAT3 diminishes tumour growth and survival in both animal and human studies. This suggests that abolishing STAT3 activity may be an effective cancer therapeutic strategy. However, despite this potential as a therapeutic target, and the extensive attempts by many laboratories and pharmaceutical companies to develop an effective STAT3 inhibitor for use in the clinic, no direct STAT3 inhibitor has been approved for clinical use. In this review, we focus on the role of STAT3 in tumorigenesis, and discuss its potential as a therapeutic target for cancer treatment.
dc.description.sponsorshipM.S.W. is supported by a UK Biotechnology and Biological Sciences Research Council CASE PhD studentship in collaboration with GlaxoSmithKline.
dc.languageEnglishen
dc.language.isoenen
dc.publisherWiley
dc.subjectcancer therapeuticsen
dc.subjectcanceren
dc.subjectinhibitorsen
dc.subjectsignallingen
dc.subjectSTAT3en
dc.subjecttumourigenesisen
dc.titleSTAT3 the oncogene – still eluding therapy?en
dc.typeArticle
dc.description.versionThis is the final version of the article. It first appeared from Wiley via http://dx.doi.org/10.1111/febs.13285en
prism.endingPage2611
prism.publicationDate2015en
prism.publicationNameFEBS Journalen
prism.startingPage2600
prism.volume282en
dc.rioxxterms.funderBBSRC
dcterms.dateAccepted2015-03-26en
rioxxterms.versionofrecord10.1111/febs.13285en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2015-04-22en
dc.contributor.orcidWatson, Christine [0000-0002-8548-5902]
dc.identifier.eissn1742-4658
rioxxterms.typeJournal Article/Reviewen
rioxxterms.freetoread.startdate2016-04-22


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