期刊
CELL REPORTS
卷 13, 期 11, 页码 2395-2402出版社
CELL PRESS
DOI: 10.1016/j.celrep.2015.11.047
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资金
- NIH [P30 CA016672, CA109298, UH3TR000943, P50 CA083639, P50 CA098258, U54 CA151668, U24CA143835]
- CPRIT [RP110595]
- Ovarian Cancer Research Fund
- United States DOD [OC073399, W81XWH-10-1-0158, BC085265]
- Marcus Foundation
- Red and Charline McCombs Institute for the Early Detection and Treatment of Cancer
- RGK Foundation
- Gilder Foundation
- Blanton-Davis Ovarian Cancer Research Program
- Betty Anne Asche Murray Distinguished Professorship
- Russell and Diana Hawkins Family Foundation Discovery Fellowship
- Foundation for Women's Cancer
- Cancer Prevention and Research Institute of Texas training grants [RP101502, RP101489]
- Deutsche Forschungsgemeinschaft (DFG)
Long noncoding RNAs (lncRNAs) significantly influence the development and regulation of genome expression in cells. Here, we demonstrate the role of lncRNA ceruloplasmin (NRCP) in cancer metabolism and elucidate functional effects leading to increased tumor progression. NRCP was highly upregulated in ovarian tumors, and knockdown of NRCP resulted in significantly increased apoptosis, decreased cell proliferation, and decreased glycolysis compared with control cancer cells. In an orthotopic mouse model of ovarian cancer, siNRCP delivered via a liposomal carrier significantly reduced tumor growth compared with control treatment. We identified NRCP as an intermediate binding partner between STAT1 and RNA polymerase II, leading to increased expression of downstream target genes such as glucose-6-phosphate isomerase. Collectively, we report a previously unrecognized role of the lncRNA NRCP in modulating cancer metabolism. As demonstrated, DOPC nanoparticle-incorporated siRNA-mediated silencing of this lncRNA in vivo provides therapeutic avenue toward modulating lncRNAs in cancer.
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