Ionizing radiation-inducible miR-30e promotes glioma cell invasion through EGFR stabilization by directly targeting CBL-B
- Authors
- Kwak, Seo-Young; Kim, Bu-Yeon; Ahn, Hyun-Joo; Yoo, Je-Ok; Kim, Joon; Bae, In Hwa; Han, Young-Hoon
- Issue Date
- 4월-2015
- Publisher
- WILEY
- Keywords
- CBL-B; EGFR; invasion; miR-30e; MMP-2
- Citation
- FEBS JOURNAL, v.282, no.8, pp.1512 - 1525
- Indexed
- SCOPUS
- Journal Title
- FEBS JOURNAL
- Volume
- 282
- Number
- 8
- Start Page
- 1512
- End Page
- 1525
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/93944
- DOI
- 10.1111/febs.13238
- ISSN
- 1742-464X
- Abstract
- MicroRNAs (miRNAs) are small non-coding RNA molecules that regulate gene expression at the transcriptional and post-transcriptional levels. Here we show that miR-30e, which was previously identified as an ionizing radiation-inducible miRNA, enhances cellular invasion by promoting secretion of the matrix metalloproteinase MMP-2. The enhancement of cellular invasion by miR-30e involved up-regulation of the epidermal growth factor receptor (EGFR) and subsequent activation of its downstream signaling mediators, AKT and extracellular signal-regulated kinase. EGFR up-regulation by miR-30e occurred due to stabilization of the EGFR protein. The E3 ubiquitin ligase casitas B-lineage lymphomaB (CBL-B) was down-regulated by miR-30e, and this led to increased EGFR abundance. A 3 UTR reporter assay confirmed that CBL-B is a direct target of miR-30e. Knocking down CBL-B expression phenocopied the effects of miR-30e, whereas ectopic expression of CBL-B suppressed miR-30e-induced EGFR up-regulation and invasion. Collectively, our results suggest that targeting miR-30e may limit the invasiveness induced during glioma radiotherapy.
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Collections - Graduate School > Department of Life Sciences > 1. Journal Articles
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