miR-122 removal in the liver activates imprinted microRNAs and enables more effective microRNA-mediated gene repressionopen access
- Authors
- Valdmanis, Paul N.; Kim, Hak Kyun; Chu, Kirk; Zhang, Feijie; Xu, Jianpeng; Munding, Elizabeth M.; Shen, Jia; Kay, Mark A.
- Issue Date
- Dec-2018
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- NATURE COMMUNICATIONS, v.9, no.1
- Journal Title
- NATURE COMMUNICATIONS
- Volume
- 9
- Number
- 1
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/63816
- DOI
- 10.1038/s41467-018-07786-7
- ISSN
- 2041-1723
- Abstract
- miR-122 is a highly expressed liver microRNA that is activated perinatally and aids in regulating cholesterol metabolism and promoting terminal differentiation of hepatocytes. Disrupting expression of miR-122 can re-activate embryo-expressed adult-silenced genes, ultimately leading to the development of hepatocellular carcinoma (HCC). Here we interrogate the liver transcriptome at various time points after genomic excision of miR-122 to determine the cellular consequences leading to oncogenesis. Loss of miR-122 leads to specific and progressive increases in expression of imprinted clusters of microRNAs and mRNA transcripts at the Igf2 and Dlk1-Dio3 loci that could be curbed by re-introduction of exogenous miR-122. mRNA targets of other abundant hepatic microRNAs are functionally repressed leading to widespread hepatic transcriptional de-regulation. Together, this reveals a transcriptomic framework for the hepatic response to loss of miR-122 and the outcome on other microRNAs and their cognate gene targets.
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Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
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