PTEN/PTENP1: 'Regulating the regulator of RTK-dependent PI3K/Akt signalling', new targets for cancer therapy

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

PTEN/PTENP1: 'Regulating the regulator of RTK-dependent PI3K/Akt signalling', new targets for cancer therapy

Haddadi, N Lin, Y

Travis, G Simpson, AM

McGowan, EM

Nassif, NT

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Publication Type:: Journal Article
Citation:: Molecular Cancer, 2018, 17 (1)
Issue Date:: 2018-02-19

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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	Travis, G	en_US
dc.contributor.author	Simpson, AM https://orcid.org/0000-0002-2249-5097	en_US
dc.contributor.author	McGowan, EM https://orcid.org/0000-0001-6371-3751	en_US
dc.contributor.author	Nassif, NT https://orcid.org/0000-0003-2675-8322	en_US
dc.date.available	2018-02-02	en_US
dc.date.issued	2018-02-19	en_US
dc.identifier.citation	Molecular Cancer, 2018, 17 (1)	en_US
dc.identifier.uri	http://hdl.handle.net/10453/125870
dc.description.abstract	© 2018 The Author(s). Regulation of the PI-3 kinase (PI3K)/Akt signalling pathway is essential for maintaining the integrity of fundamental cellular processes, cell growth, survival, death and metabolism, and dysregulation of this pathway is implicated in the development and progression of cancers. Receptor tyrosine kinases (RTKs) are major upstream regulators of PI3K/Akt signalling. The phosphatase and tensin homologue (PTEN), a well characterised tumour suppressor, is a prime antagonist of PI3K and therefore a negative regulator of this pathway. Loss or inactivation of PTEN, which occurs in many tumour types, leads to overactivation of RTK/PI3K/Akt signalling driving tumourigenesis. Cellular PTEN levels are tightly regulated by a number of transcriptional, post-transcriptional and post-translational regulatory mechanisms. Of particular interest, transcription of the PTEN pseudogene, PTENP1, produces sense and antisense transcripts that exhibit post-transcriptional and transcriptional modulation of PTEN expression respectively. These additional levels of regulatory complexity governing PTEN expression add to the overall intricacies of the regulation of RTK/PI-3K/Akt signalling. This review will discuss the regulation of oncogenic PI3K signalling by PTEN (the regulator) with a focus on the modulatory effects of the sense and antisense transcripts of PTENP1 on PTEN expression, and will further explore the potential for new therapeutic opportunities in cancer treatment.	en_US
dc.relation.ispartof	Molecular Cancer	en_US
dc.relation.isbasedon	10.1186/s12943-018-0803-3	en_US
dc.subject.classification	Oncology & Carcinogenesis	en_US
dc.subject.mesh	Animals	en_US
dc.subject.mesh	Humans	en_US
dc.subject.mesh	Neoplasms	en_US
dc.subject.mesh	MicroRNAs	en_US
dc.subject.mesh	Antineoplastic Agents	en_US
dc.subject.mesh	Signal Transduction	en_US
dc.subject.mesh	Proto-Oncogene Proteins c-akt	en_US
dc.subject.mesh	PTEN Phosphohydrolase	en_US
dc.subject.mesh	Protein-Tyrosine Kinases	en_US
dc.subject.mesh	Phosphatidylinositol 3-Kinases	en_US
dc.title	PTEN/PTENP1: 'Regulating the regulator of RTK-dependent PI3K/Akt signalling', new targets for cancer therapy	en_US
dc.type	Journal Article
utslib.citation.volume	1	en_US
utslib.citation.volume	17	en_US
utslib.for	1112 Oncology and Carcinogenesis	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	1	en_US
pubs.publication-status	Published	en_US
pubs.volume	17	en_US

Abstract:

© 2018 The Author(s). Regulation of the PI-3 kinase (PI3K)/Akt signalling pathway is essential for maintaining the integrity of fundamental cellular processes, cell growth, survival, death and metabolism, and dysregulation of this pathway is implicated in the development and progression of cancers. Receptor tyrosine kinases (RTKs) are major upstream regulators of PI3K/Akt signalling. The phosphatase and tensin homologue (PTEN), a well characterised tumour suppressor, is a prime antagonist of PI3K and therefore a negative regulator of this pathway. Loss or inactivation of PTEN, which occurs in many tumour types, leads to overactivation of RTK/PI3K/Akt signalling driving tumourigenesis. Cellular PTEN levels are tightly regulated by a number of transcriptional, post-transcriptional and post-translational regulatory mechanisms. Of particular interest, transcription of the PTEN pseudogene, PTENP1, produces sense and antisense transcripts that exhibit post-transcriptional and transcriptional modulation of PTEN expression respectively. These additional levels of regulatory complexity governing PTEN expression add to the overall intricacies of the regulation of RTK/PI-3K/Akt signalling. This review will discuss the regulation of oncogenic PI3K signalling by PTEN (the regulator) with a focus on the modulatory effects of the sense and antisense transcripts of PTENP1 on PTEN expression, and will further explore the potential for new therapeutic opportunities in cancer treatment.

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

http://hdl.handle.net/10453/122336