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Article: Suppression of p16 Induces mTORC1-Mediated Nucleotide Metabolic Reprogramming

TitleSuppression of p16 Induces mTORC1-Mediated Nucleotide Metabolic Reprogramming
Authors
Buj, RaquelChen, Chi WeiDahl, Erika S.Leon, Kelly E.Kuskovsky, RostislavMaglakelidze, NatellaNavaratnarajah, MaithiliZhang, GaoDoan, Mary T.Jiang, HelenZaleski, MichaelKutzler, LydiaLacko, HollyLu, YilingMills, Gordon B.Gowda, RaghavendraRobertson, Gavin P.Warrick, Joshua I.Herlyn, MeenhardImamura, YukaKimball, Scot R.DeGraff, David J.Snyder, Nathaniel W.Aird, Katherine M.
KeywordsBRAF
cancer metabolism
cell cycle
melanoma
nevi
pancreatic cancer
pentose phosphate pathway
ribonucleotide reductase M2
ribose-5-phosphate isomerase A
senescence
Issue Date2019
Citation
Cell Reports, 2019, v. 28, n. 8, p. 1971-1980.e8 How to Cite?
DOI: http://dx.doi.org/10.1016/j.celrep.2019.07.084
AbstractSenescence bypass through p16 loss predisposes to transformation and tumorigenesis. Buj et al. found that the loss of p16 upregulates nucleotide metabolism through increased mTORC1-mediated translation of RPIA to bypass senescence in an RB-independent manner. Thus, the mTORC1-RPIA axis is a metabolic vulnerability for p16-null cancers.
Persistent Identifierhttp://hdl.handle.net/10722/318782
PubMed Central ID
PMC6716532
ISI Accession Number ID
WOS:000482135400003

 

DC FieldValueLanguage
dc.contributor.authorBuj, Raquel-
dc.contributor.authorChen, Chi Wei-
dc.contributor.authorDahl, Erika S.-
dc.contributor.authorLeon, Kelly E.-
dc.contributor.authorKuskovsky, Rostislav-
dc.contributor.authorMaglakelidze, Natella-
dc.contributor.authorNavaratnarajah, Maithili-
dc.contributor.authorZhang, Gao-
dc.contributor.authorDoan, Mary T.-
dc.contributor.authorJiang, Helen-
dc.contributor.authorZaleski, Michael-
dc.contributor.authorKutzler, Lydia-
dc.contributor.authorLacko, Holly-
dc.contributor.authorLu, Yiling-
dc.contributor.authorMills, Gordon B.-
dc.contributor.authorGowda, Raghavendra-
dc.contributor.authorRobertson, Gavin P.-
dc.contributor.authorWarrick, Joshua I.-
dc.contributor.authorHerlyn, Meenhard-
dc.contributor.authorImamura, Yuka-
dc.contributor.authorKimball, Scot R.-
dc.contributor.authorDeGraff, David J.-
dc.contributor.authorSnyder, Nathaniel W.-
dc.contributor.authorAird, Katherine M.-
dc.date.accessioned2022-10-11T12:24:33Z-
dc.date.available2022-10-11T12:24:33Z-
dc.date.issued2019-
dc.identifier.citationCell Reports, 2019, v. 28, n. 8, p. 1971-1980.e8-
dc.identifier.urihttp://hdl.handle.net/10722/318782-
dc.description.abstractSenescence bypass through p16 loss predisposes to transformation and tumorigenesis. Buj et al. found that the loss of p16 upregulates nucleotide metabolism through increased mTORC1-mediated translation of RPIA to bypass senescence in an RB-independent manner. Thus, the mTORC1-RPIA axis is a metabolic vulnerability for p16-null cancers.-
dc.languageeng-
dc.relation.ispartofCell Reports-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectBRAF-
dc.subjectcancer metabolism-
dc.subjectcell cycle-
dc.subjectmelanoma-
dc.subjectnevi-
dc.subjectpancreatic cancer-
dc.subjectpentose phosphate pathway-
dc.subjectribonucleotide reductase M2-
dc.subjectribose-5-phosphate isomerase A-
dc.subjectsenescence-
dc.titleSuppression of p16 Induces mTORC1-Mediated Nucleotide Metabolic Reprogramming-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1016/j.celrep.2019.07.084-
dc.identifier.pmid31433975-
dc.identifier.pmcidPMC6716532-
dc.identifier.scopuseid_2-s2.0-85070554726-
dc.identifier.volume28-
dc.identifier.issue8-
dc.identifier.spage1971-
dc.identifier.epage1980.e8-
dc.identifier.eissn2211-1247-
dc.identifier.isiWOS:000482135400003-

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