期刊
CELL SYSTEMS
卷 7, 期 1, 页码 77-+出版社
CELL PRESS
DOI: 10.1016/j.cels.2018.05.019
关键词
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资金
- National Breast Cancer Foundation [CG-10-04, ECF-14-043]
- Australian Research Council Center of Excellence in Convergent Bio-Nano Science and Technology [CE140100036]
- Australian National Health and Medical Research Council [GNT1068773, GNT1034633, GNT1069128, GNT1026191, GNT1118170]
- Melbourne International Fee Remission Scholarship (MIFRS)
- Melbourne International Research Scholarship (MIRS)
- Cancer Council SA Beat Cancer Fellowship
- Florey Fellowship from the Royal Adelaide Hospital Research Foundation
- National Breast Cancer Foundation [CG-10-04] Funding Source: researchfish
MicroRNAs (miRNAs) are important post-transcriptional regulators of gene expression, functioning in part by facilitating the degradation of target mRNAs. They have an established role in controlling epithelial- mesenchymal transition (EMT), a reversible phenotypic program underlying normal and pathological processes. Many studies demonstrate the role of individual miRNAs using overexpression at levels greatly exceeding physiological abundance. This can influence transcripts with relatively poor targeting and may in part explain why over 130 different miRNAs are directly implicated as EMT regulators. Analyzing a human mammary cell model of EMT we found evidence that a set of miRNAs, including the miR-200 and miR-182/183 family members, cooperate in post-transcriptional regulation, both reinforcing and buffering transcriptional output. Investigating this, we demonstrate that combinatorial treatment altered cellular phenotype with miRNA concentrations much closer to endogenous levels and with less off-target effects. This suggests that co-operative targeting by miRNAs is important for their physiological function and future work classifying miRNAs should consider such combinatorial effects.
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