Please use this identifier to cite or link to this item:
https://doi.org/10.1371/journal.pone.0013545
DC Field | Value | |
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dc.title | Alkylation of the tumor suppressor PTEN activates Akt and β-catenin signaling: A mechanism linking inflammation and oxidative stress with cancer | |
dc.contributor.author | Covey, T.M. | |
dc.contributor.author | Edes, K. | |
dc.contributor.author | Coombs, G.S. | |
dc.contributor.author | Virshup, D.M. | |
dc.contributor.author | Fitzpatrick, F.A. | |
dc.date.accessioned | 2016-06-01T10:24:38Z | |
dc.date.available | 2016-06-01T10:24:38Z | |
dc.date.issued | 2010 | |
dc.identifier.citation | Covey, T.M., Edes, K., Coombs, G.S., Virshup, D.M., Fitzpatrick, F.A. (2010). Alkylation of the tumor suppressor PTEN activates Akt and β-catenin signaling: A mechanism linking inflammation and oxidative stress with cancer. PLoS ONE 5 (10) : -. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0013545 | |
dc.identifier.issn | 19326203 | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/124645 | |
dc.description.abstract | PTEN, a phosphoinositide-3-phosphatase, serves dual roles as a tumor suppressor and regulator of cellular anabolic/catabolic metabolism. Adaptation of a redox-sensitive cysteinyl thiol in PTEN for signal transduction by hydrogen peroxide may have superimposed a vulnerability to other mediators of oxidative stress and inflammation, especially reactive carbonyl species, which are commonly occurring by-products of arachidonic acid peroxidation. Using MCF7 and HEK-293 cells, we report that several reactive aldehydes and ketones, e.g. electrophilic α,β-enals (acrolein, 4-hydroxy-2-nonenal) and α,β- enones (prostaglandin A2, Δ12-prostaglandin J2 and 15-deoxy-Δ-12,14-prostaglandin J2) covalently modify and inactivate cellular PTEN, with ensuing activation of PKB/Akt kinase; phosphorylation of Akt substrates; increased cell proliferation; and increased nuclear β-catenin signaling. Alkylation of PTEN by α,β-enals/enones and interference with its restraint of cellular PKB/Akt signaling may accentuate hyperplastic and neoplastic disorders associated with chronic inflammation, oxidative stress, or aging. © 2010 Covey et al. | |
dc.description.uri | http://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1371/journal.pone.0013545 | |
dc.source | Scopus | |
dc.type | Article | |
dc.contributor.department | DUKE-NUS GRADUATE MEDICAL SCHOOL S'PORE | |
dc.description.doi | 10.1371/journal.pone.0013545 | |
dc.description.sourcetitle | PLoS ONE | |
dc.description.volume | 5 | |
dc.description.issue | 10 | |
dc.description.page | - | |
dc.identifier.isiut | 000283293800014 | |
Appears in Collections: | Staff Publications Elements |
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2010-alkylation_tumor_suppressor_PTEN-published.pdf | 3.13 MB | Adobe PDF | OPEN | Published | View/Download |
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