Journal
CANCER CELL
Volume 26, Issue 3, Pages 344-357Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2014.07.009
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Funding
- Basser Research Center for BRCA
- NIH [R01CA142776, P50CA083638, P50CA083639, P50CA098258, U24CA143883, P01CA099031, R01CA127334, R01CA148759, K12HD000849]
- Ovarian Cancer Research Fund
- Breast Cancer Alliance
- Department of Defense
- Marsha Rivkin Center for Ovarian Cancer Research
- China Scholarship Council
- NIH Cancer Center through the MD Anderson Cancer Center [CA016672]
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In a genome-wide survey on somatic copy-number alterations (SCNAs) of long noncoding RNA (IncRNA) in 2,394 tumor specimens from 12 cancer types, we found that about 21.8% of IncRNA genes were located in regions with focal SCNAs. By integrating bioinformatics analyses of IncRNA SCNAs and expression with functional screening assays, we identified an oncogene, focally amplified IncRNA on chromosome 1 (FAL1), whose copy number and expression are correlated with outcomes in ovarian cancer. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo.
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