Abstract:
:Somatic mutations in the RNase IIIb domain of DICER1 arise in cancer and disrupt the cleavage of 5' pre-miRNA arms. Here, we characterize an unstudied, recurrent, mutation (S1344L) in the DICER1 RNase IIIa domain in tumors from The Cancer Genome Atlas (TCGA) project and MSK-IMPACT profiling. RNase IIIa/b hotspots are absent from most cancers, but are notably enriched in uterine cancers. Systematic analysis of TCGA small RNA datasets show that DICER1 RNase IIIa-S1344L tumors deplete 5p-miRNAs, analogous to RNase IIIb hotspot samples. Structural and evolutionary coupling analyses reveal constrained proximity of RNase IIIa-S1344 to the RNase IIIb catalytic site, rationalizing why mutation of this site phenocopies known hotspot alterations. Finally, examination of DICER1 hotspot endometrial tumors reveals derepression of specific miRNA target signatures. In summary, comprehensive analyses of DICER1 somatic mutations and small RNA data reveal a mechanistic aspect of pre-miRNA processing that manifests in specific cancer settings.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Vedanayagam J,Chatila WK,Aksoy BA,Majumdar S,Skanderup AJ,Demir E,Schultz N,Sander C,Lai ECdoi
10.1038/s41467-019-11610-1subject
Has Abstractpub_date
2019-08-15 00:00:00pages
3682issue
1issn
2041-1723pii
10.1038/s41467-019-11610-1journal_volume
10pub_type
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