期刊
NATURE COMMUNICATIONS
卷 4, 期 -, 页码 -出版社
NATURE RESEARCH
DOI: 10.1038/ncomms3812
关键词
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资金
- NIH [R01CA070896, R01CA075503, R01CA132115, R01CA107382, R01CA086072]
- National Basic Research Program of China [2012CB966800]
- NSFC [81172515]
- Kimmel Cancer Center NIH Cancer Center Core [P30CA056036]
- Dr. Ralph and Marian C. Falk Medical Research Trust
- Pennsylvania Department of Health
Cyclin D1 encodes the regulatory subunit of a holoenzyme that phosphorylates the pRB protein and promotes G(1)/S cell-cycle progression and oncogenesis. Dicer is a central regulator of miRNA maturation, encoding an enzyme that cleaves double-stranded RNA or stem-loop-stem RNA into 20-25 nucleotide long small RNA, governing sequence-specific gene silencing and heterochromatin methylation. The mechanism by which the cell cycle directly controls the non-coding genome is poorly understood. Here we show that cyclin D1(-/-) cells are defective in pre-miRNA processing which is restored by cyclin D1a rescue. Cyclin D1 induces Dicer expression in vitro and in vivo. Dicer is transcriptionally targeted by cyclin D1, via a cdk-independent mechanism. Cyclin D1 and Dicer expression significantly correlates in luminal A and basal-like subtypes of human breast cancer. Cyclin D1 and Dicer maintain heterochromatic histone modification (Tri-m-H3K9). Cyclin D1-mediated cellular proliferation and migration is Dicer-dependent. We conclude that cyclin D1 induction of Dicer coordinates microRNA biogenesis.
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