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Article: Transketolase counteracts oxidative stress to drive cancer development

TitleTransketolase counteracts oxidative stress to drive cancer development
Authors
Issue Date2016
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings of the National Academy of Sciences, 2016, v. 113 n. 6, p. E725-E734 How to Cite?
AbstractCancer cells experience an increase in oxidative stress. The pentose phosphate pathway (PPP) is a major biochemical pathway that generates antioxidant NADPH. Here, we show that transketolase (TKT), an enzyme in the PPP, is required for cancer growth because of its ability to affect the production of NAPDH to counteract oxidative stress. We show that TKT expression is tightly regulated by the Nuclear Factor, Erythroid 2-Like 2 (NRF2)/Kelch-Like ECH-Associated Protein 1 (KEAP1)/BTB and CNC Homolog 1 (BACH1) oxidative stress sensor pathway in cancers. Disturbing the redox homeostasis of cancer cells by genetic knockdown or pharmacologic inhibition of TKT sensitizes cancer cells to existing targeted therapy (Sorafenib). Our study strengthens the notion that antioxidants are beneficial to cancer growth and highlights the therapeutic benefits of targeting pathways that generate antioxidants.
Persistent Identifierhttp://hdl.handle.net/10722/232164
ISSN
2015 Impact Factor: 9.423
2015 SCImago Journal Rankings: 6.883
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorXu, M-
dc.contributor.authorLai, KH-
dc.contributor.authorLin, SH-
dc.contributor.authorTse, PW-
dc.contributor.authorChiu, KC-
dc.contributor.authorKoh, HY-
dc.contributor.authorLaw, CT-
dc.contributor.authorWong, CM-
dc.contributor.authorCai, Z-
dc.contributor.authorWong, CCL-
dc.contributor.authorNg, IOL-
dc.date.accessioned2016-09-20T05:28:10Z-
dc.date.available2016-09-20T05:28:10Z-
dc.date.issued2016-
dc.identifier.citationProceedings of the National Academy of Sciences, 2016, v. 113 n. 6, p. E725-E734-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/232164-
dc.description.abstractCancer cells experience an increase in oxidative stress. The pentose phosphate pathway (PPP) is a major biochemical pathway that generates antioxidant NADPH. Here, we show that transketolase (TKT), an enzyme in the PPP, is required for cancer growth because of its ability to affect the production of NAPDH to counteract oxidative stress. We show that TKT expression is tightly regulated by the Nuclear Factor, Erythroid 2-Like 2 (NRF2)/Kelch-Like ECH-Associated Protein 1 (KEAP1)/BTB and CNC Homolog 1 (BACH1) oxidative stress sensor pathway in cancers. Disturbing the redox homeostasis of cancer cells by genetic knockdown or pharmacologic inhibition of TKT sensitizes cancer cells to existing targeted therapy (Sorafenib). Our study strengthens the notion that antioxidants are beneficial to cancer growth and highlights the therapeutic benefits of targeting pathways that generate antioxidants.-
dc.languageeng-
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org-
dc.relation.ispartofProceedings of the National Academy of Sciences-
dc.rightsProceedings of the National Academy of Sciences. Copyright © National Academy of Sciences.-
dc.titleTransketolase counteracts oxidative stress to drive cancer development-
dc.typeArticle-
dc.identifier.emailTse, PW: akipwtse@hku.hk-
dc.identifier.emailKoh, HY: huiyukoh@hku.hk-
dc.identifier.emailWong, CM: jcmwong@hku.hk-
dc.identifier.emailWong, CCL: carmencl@pathology.hku.hk-
dc.identifier.emailNg, IOL: iolng@hku.hk-
dc.identifier.authorityWong, CM=rp00231-
dc.identifier.authorityWong, CCL=rp01602-
dc.identifier.authorityNg, IOL=rp00335-
dc.identifier.doi10.1073/pnas.1508779113-
dc.identifier.pmcidPMC4760787-
dc.identifier.hkuros264757-
dc.identifier.volume113-
dc.identifier.issue6-
dc.identifier.spageE725-
dc.identifier.epageE734-
dc.publisher.placeUnited States-

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