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dc.contributor.authorPohl, S.
dc.contributor.authorScott, R.
dc.contributor.authorArfuso, Frank
dc.contributor.authorPerumal, V.
dc.contributor.authorDharmarajan, Arunasalam
dc.date.accessioned2017-01-30T12:03:24Z
dc.date.available2017-01-30T12:03:24Z
dc.date.created2015-10-29T04:09:51Z
dc.date.issued2015
dc.identifier.citationPohl, S. and Scott, R. and Arfuso, F. and Perumal, V. and Dharmarajan, A. 2015. Secreted frizzled-related protein 4 and its implications in cancer and apoptosis. Tumor Biology. 36 (1): pp. 143-152.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/17677
dc.identifier.doi10.1007/s13277-014-2956-z
dc.description.abstract

Secreted frizzled-related protein 4 (SFRP4) is a glycoprotein that acts as an antagonist of Wnt ligands, causing inhibition of the canonical Wnt signalling pathway. First noticed due to high expression levels during times of increased apoptosis, SFRP4 has been implicated in cell proliferation and differentiation and plays an important role in carcinogenesis. Many tumours such as endometrial, cervical, ovarian, prostate, bladder, colorectal, mesothelioma, pancreatic, renal, and oesophageal tumours are characterised by aberrant promoter hypermethylation, which causes variations in the expression level of SFRP4 when compared to normal cells. Combined experimental data appear to confirm the suggested role of SFRP4 as a local initiator of apoptosis; however, increased SFRP4 expression may not always correlate with an increase in apoptosis, possibly due to the complex interactions between different signalling pathways. SFRP4 can be explored for its use in novel therapeutic modalities as well as being a potential diagnostic biomarker.

dc.publisherKluwer Academic Publishers
dc.titleSecreted frizzled-related protein 4 and its implications in cancer and apoptosis
dc.typeJournal Article
dcterms.source.volume36
dcterms.source.number1
dcterms.source.startPage143
dcterms.source.endPage152
dcterms.source.issn1010-4283
dcterms.source.titleTumor Biology
curtin.departmentSchool of Biomedical Sciences
curtin.accessStatusFulltext not available


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