Show simple item record

dc.contributor.authorKoundouros, Nen_US
dc.contributor.authorPoulogiannis, Gen_US
dc.coverage.spatialSwitzerlanden_US
dc.date.accessioned2019-03-05T10:52:37Z
dc.date.issued2018en_US
dc.identifierhttps://www.ncbi.nlm.nih.gov/pubmed/29868481en_US
dc.identifier.citationFront Oncol, 2018, 8 pp. 160 - ?en_US
dc.identifier.issn2234-943Xen_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3134
dc.identifier.doi10.3389/fonc.2018.00160en_US
dc.description.abstractMetabolic rewiring and the consequent production of reactive oxygen species (ROS) are necessary to promote tumorigenesis. At the nexus of these cellular processes is the aberrant regulation of oncogenic signaling cascades such as the phosphoinositide 3-kinase and AKT (PI3K/Akt) pathway, which is one of the most frequently dysregulated pathways in cancer. In this review, we examine the regulation of ROS metabolism in the context of PI3K-driven tumors with particular emphasis on four main areas of research. (1) Stimulation of ROS production through direct modulation of mitochondrial bioenergetics, activation of NADPH oxidases (NOXs), and metabolic byproducts associated with hyperactive PI3K/Akt signaling. (2) The induction of pro-tumorigenic signaling cascades by ROS as a consequence of phosphatase and tensin homolog and receptor tyrosine phosphatase redox-dependent inactivation. (3) The mechanisms through which PI3K/Akt activation confers a selective advantage to cancer cells by maintaining redox homeostasis. (4) Opportunities for therapeutically exploiting redox metabolism in PIK3CA mutant tumors and the potential for implementing novel combinatorial therapies to suppress tumor growth and overcome drug resistance. Further research focusing on the multi-faceted interactions between PI3K/Akt signaling and ROS metabolism will undoubtedly contribute to novel insights into the extensive pro-oncogenic effects of this pathway, and the identification of exploitable vulnerabilities for the treatment of hyperactive PI3K/Akt tumors.en_US
dc.format.extent160 - ?en_US
dc.languageengen_US
dc.language.isoengen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.subjectcanceren_US
dc.subjectmetabolismen_US
dc.subjectoxidative stressen_US
dc.subjectphosphoinositide 3-kinase/Akt signalingen_US
dc.subjectreactive oxygen speciesen_US
dc.titlePhosphoinositide 3-Kinase/Akt Signaling and Redox Metabolism in Cancer.en_US
dc.typeJournal Article
dcterms.dateAccepted2018-04-26en_US
rioxxterms.versionofrecord10.3389/fonc.2018.00160en_US
rioxxterms.licenseref.startdate2018en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfFront Oncolen_US
pubs.notesNot knownen_US
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Signalling & Cancer Metabolism
pubs.publication-statusPublished onlineen_US
pubs.volume8en_US
pubs.embargo.termsNot knownen_US
icr.researchteamSignalling & Cancer Metabolismen_US
dc.contributor.icrauthorPoulogiannis, Georgiosen_US


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record

http://creativecommons.org/licenses/by/4.0/
Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by/4.0/