“Dicing and splicing” sphingosine kinase and relevance to cancer

Haddadi, N; Lin, Y; Simpson, AM; Nassif, NT; McGowan, EM

“Dicing and splicing” sphingosine kinase and relevance to cancer

Haddadi, N Lin, Y

Simpson, AM

Nassif, NT

McGowan, EM

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Publication Type:: Journal Article
Citation:: International Journal of Molecular Sciences, 2017, 18 (9)
Issue Date:: 2017-09-02

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Field	Value	Language
dc.contributor.author	Haddadi, N	en_US
dc.contributor.author	Lin, Y https://orcid.org/0000-0002-4637-9701	en_US
dc.contributor.author	Simpson, AM https://orcid.org/0000-0002-2249-5097	en_US
dc.contributor.author	Nassif, NT https://orcid.org/0000-0003-2675-8322	en_US
dc.contributor.author	McGowan, EM https://orcid.org/0000-0001-6371-3751	en_US
dc.date.available	2017-08-28	en_US
dc.date.issued	2017-09-02	en_US
dc.identifier.citation	International Journal of Molecular Sciences, 2017, 18 (9)	en_US
dc.identifier.issn	1661-6596	en_US
dc.identifier.uri	http://hdl.handle.net/10453/116444
dc.description.abstract	© 2017 by the authors. Licensee MDPI, Basel, Switzerland. Sphingosine kinase (SphK) is a lipid enzyme that maintains cellular lipid homeostasis. Two SphK isozymes, SphK1 and SphK2, are expressed from different chromosomes and several variant isoforms are expressed from each of the isozymes, allowing for the multi-faceted biological diversity of SphK activity. Historically, SphK1 is mainly associated with oncogenicity, however in reality, both SphK1 and SphK2 isozymes possess oncogenic properties and are recognized therapeutic targets. The absence of mutations of SphK in various cancer types has led to the theory that cancer cells develop a dependency on SphK signaling (hyper-SphK signaling) or “non-oncogenic addiction”. Here we discuss additional theories of SphK cellular mislocation and aberrant “dicing and splicing” as contributors to cancer cell biology and as key determinants of the success or failure of SphK/S1P (sphingosine 1 phosphate) based therapeutics.	en_US
dc.relation.ispartof	International Journal of Molecular Sciences	en_US
dc.relation.isbasedon	10.3390/ijms18091891	en_US
dc.subject.classification	Chemical Physics	en_US
dc.subject.mesh	Animals	en_US
dc.subject.mesh	Humans	en_US
dc.subject.mesh	Neoplasms	en_US
dc.subject.mesh	Disease Models, Animal	en_US
dc.subject.mesh	Sphingosine	en_US
dc.subject.mesh	Isoenzymes	en_US
dc.subject.mesh	Phosphotransferases (Alcohol Group Acceptor)	en_US
dc.subject.mesh	Lysophospholipids	en_US
dc.subject.mesh	Receptors, Lysosphingolipid	en_US
dc.subject.mesh	Evolution, Molecular	en_US
dc.subject.mesh	Signal Transduction	en_US
dc.subject.mesh	Gene Expression Regulation, Neoplastic	en_US
dc.subject.mesh	RNA Splicing	en_US
dc.subject.mesh	Protein Transport	en_US
dc.subject.mesh	Multigene Family	en_US
dc.title	“Dicing and splicing” sphingosine kinase and relevance to cancer	en_US
dc.type	Journal Article
utslib.citation.volume	9	en_US
utslib.citation.volume	18	en_US
utslib.for	0399 Other Chemical Sciences	en_US
utslib.for	0604 Genetics	en_US
utslib.for	0699 Other Biological Sciences	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
utslib.copyright.status	open_access
pubs.issue	9	en_US
pubs.publication-status	Published	en_US
pubs.volume	18	en_US

Abstract:

© 2017 by the authors. Licensee MDPI, Basel, Switzerland. Sphingosine kinase (SphK) is a lipid enzyme that maintains cellular lipid homeostasis. Two SphK isozymes, SphK1 and SphK2, are expressed from different chromosomes and several variant isoforms are expressed from each of the isozymes, allowing for the multi-faceted biological diversity of SphK activity. Historically, SphK1 is mainly associated with oncogenicity, however in reality, both SphK1 and SphK2 isozymes possess oncogenic properties and are recognized therapeutic targets. The absence of mutations of SphK in various cancer types has led to the theory that cancer cells develop a dependency on SphK signaling (hyper-SphK signaling) or “non-oncogenic addiction”. Here we discuss additional theories of SphK cellular mislocation and aberrant “dicing and splicing” as contributors to cancer cell biology and as key determinants of the success or failure of SphK/S1P (sphingosine 1 phosphate) based therapeutics.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/116444