期刊
MOLECULAR CELL
卷 61, 期 4, 页码 520-534出版社
CELL PRESS
DOI: 10.1016/j.molcel.2016.01.015
关键词
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资金
- NIH/NCI [1UH2TR00943-01, 1 R01 CA182905-01]
- NCI [P50 CA093459]
- Aim at Melanoma Foundation
- Miriam and Jim Mulva research funds
- Brain SPORE [2P50CA127001]
- Center for Radiation Oncology Research Project
- Center for Cancer Epigenetics Pilot project
- Knowledge GAP MDACC grant
- CLL Moonshot pilot project
- UT MD Anderson Cancer Center Duncan Family Institute for Cancer Prevention and Risk Assessment
- SINF grant in colon cancer
- Laura and John Arnold Foundation
- RGK Foundation
- Sao Paulo Research Foundation FAPESP [2014/15968-3, 2014/20673-2, 2014/17820-3]
- University of Texas MD Anderson Cancer Center Sheikh Ahmed Bin Zayed Al Nahyan Center for Pancreatic Cancer Research
- Cancer Center Support Grant [P30 CA016672]
- Cancer Prevention and Research Institutes of Texas [RP-101243P5]
- NIH/NCI from the Cancer Prevention and Research Institute of Texas [R01CA175486, RP140462]
- Jeanne F. Shelby Scholarship Fund
- Fulbright fellowship
Altered 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.
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