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dc.contributor.authorRedis, Roxana S.-
dc.contributor.authorVela, Luz E.-
dc.contributor.authorLu, Weiqin-
dc.contributor.authorFerreira de Oliveira, Juliana-
dc.contributor.authorRodriguez-Aguayo, Cristian-
dc.contributor.authorAdamoski, Douglas-
dc.contributor.authorPasculli, Barbara-
dc.contributor.authorTaguchi, Ayumu-
dc.contributor.authorChen, Yunyun-
dc.contributor.authorFernández, Agustín F.-
dc.contributor.authorValledor, Luis-
dc.contributor.authorVan Roosbroeck, Katrien-
dc.contributor.authorChang, Samuel-
dc.contributor.authorShah, Maitri-
dc.contributor.authorKinnebrew, Garrett-
dc.contributor.authorHan, Leng-
dc.contributor.authorAtlasi, Yaser-
dc.contributor.authorCheung, Lawrence H.-
dc.contributor.authorHuang, Gilbert Y.-
dc.contributor.authorMonroig, Paloma-
dc.contributor.authorRamirez, Marc S.-
dc.contributor.authorCatela, Ivkovic, Tina-
dc.contributor.authorVan, Long-
dc.contributor.authorLing, Hui-
dc.contributor.authorGafà, Roberta-
dc.contributor.authorKapitanovic, Sanja-
dc.contributor.authorLanza, Giovanni-
dc.contributor.authorBankson, James A.-
dc.contributor.authorHuang, Peng-
dc.contributor.authorLai, Stephen Y.-
dc.contributor.authorBast, Robert C.-
dc.contributor.authorRosenblum, Michael G.-
dc.contributor.authorRadovich, Milan-
dc.contributor.authorIvan, Mircea-
dc.contributor.authorBartholomeusz, Geoffrey-
dc.contributor.authorLiang, Hang-
dc.contributor.authorFraga, Mario F.-
dc.contributor.authorWidger, William R.-
dc.contributor.authorHanash, Samir-
dc.contributor.authorBerindan-Neagoe, Ioana-
dc.contributor.authorLopez-Berestein, Gabriel-
dc.contributor.authorAmbrosio, Andre L. B.-
dc.contributor.authorGomes Dias, Sandra M.-
dc.contributor.authorCalin, George A.-
dc.identifierdoi: 10.1016/j.molcel.2016.01.015-
dc.identifiere-issn: 1097-4164-
dc.identifierissn: 1097-2765-
dc.identifier.citationMolecular Cell 61(4): 520-534 (2016)-
dc.description.abstractAltered energy metabolism is a cancer hallmark as malignant cells tailor their metabolic pathways to meet their energy requirements. Glucose and glutamine are the major nutrients that fuel cellular metabolism, and the pathways utilizing these nutrients are often altered in cancer. Here, we show that the long ncRNA CCAT2, located at the 8q24 amplicon on cancer risk-associated rs6983267 SNP, regulates cancer metabolism in vitro and in vivo in an allele-specific manner by binding the Cleavage Factor I (CFIm) complex with distinct affinities for the two subunits (CFIm25 and CFIm68). The CCAT2 interaction with the CFIm complex fine-tunes the alternative splicing of Glutaminase (GLS) by selecting the poly(A) site in intron 14 of the precursor mRNA. These findings uncover a complex, allele-specific regulatory mechanism of cancer metabolism orchestrated by the two alleles of a long ncRNA.-
dc.description.sponsorshipG.A.C. is The Alan M. Gewirtz Leukemia & Lymphoma Society Scholar. Work in G.A.C.’s laboratory is supported in part by the NIH/NCI grants 1UH2TR00943-01 and 1 R01 CA182905-01, the UT MD Anderson Cancer Center SPORE in Melanoma grant from NCI (P50 CA093459), Aim at Melanoma Foundation and the Miriam and Jim Mulva research funds, the Brain SPORE (2P50CA127001), the Center for Radiation Oncology Research Project, the Center for Cancer Epigenetics Pilot project, a 2014 Knowledge GAP MDACC grant, a CLL Moonshot pilot project, the UT MD Anderson Cancer Center Duncan Family Institute for Cancer Prevention and Risk Assessment, a SINF grant in colon cancer, the Laura and John Arnold Foundation, the RGK Foundation, and the Estate of C.G. Johnson, Jr. I.B.-N. was financed by a grant entitled Non-Invasive Intelligent Systems for Colorectal Cancer Diagnosis and Prognosis Based on circulating miRNAs Integrated in the Clinical Workflow – INTELCOR. S.M.G.D., A.L.B.A., and D.A. are supported by the São Paulo Research Foundation FAPESP under grants 2014/15968-3, 2014/20673-2, and 2014/17820-3, respectively. W.L. was partly supported by grants from The University of Texas MD Anderson Cancer Center Sheikh Ahmed Bin Zayed Al Nahyan Center for Pancreatic Cancer Research. J.A.B. was supported by the Cancer Center Support Grant (P30 CA016672), and the HP imaging program of the Small Animal Facility (SAIF) was supported by the Cancer Prevention and Research Institutes of Texas grant RP-101243P5. H.L. was supported by NIH/NCI grant R01CA175486, a grant (RP140462) from the Cancer Prevention and Research Institute of Texas, and the R. Lee Clark Fellow Award from The Jeanne F. Shelby Scholarship Fund. I.B.-N. was financed by a Fulbright fellowship and by a grant entitled Non-Invasive Intelligent Systems for Colorectal Cancer Diagnosis and Prognosis Based on circulating miRNAs Integrated in the Clinical Workflow – INTELCOR.-
dc.titleAllele-specific reprogramming of cancer metabolism by the long non-coding RNA CCAT2-
dc.description.versionPeer Reviewed-
dc.contributor.funderMohamed bin Zayed Species Conservation Fund-
dc.contributor.funderUniversity of Texas-
dc.contributor.funderFundações de Amparo à Pesquisa (Brasil)-
dc.contributor.funderLeukemia & Lymphoma Society (US)-
dc.contributor.funderNational Institutes of Health (US)-
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