期刊
PLOS ONE
卷 9, 期 4, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0093441
关键词
-
资金
- NIH [4R01-CA129190, HL16037, HL70631]
beta-arrestins, ubiquitous cellular scaffolding proteins that act as signaling mediators of numerous critical cellular pathways, are attractive therapeutic targets because they promote tumorigenesis in several tumor models. However, targeting scaffolding proteins with traditional small molecule drugs has been challenging. Inhibition of beta-arrestin 2 with a novel aptamer impedes multiple oncogenic signaling pathways simultaneously. Additionally, delivery of the beta-arrestin 2-targeting aptamer into leukemia cells through coupling to a recently described cancer cell-specific delivery aptamer, inhibits multiple beta-arrestin-mediated signaling pathways known to be required for chronic myelogenous leukemia (CML) disease progression, and impairs tumorigenic growth in CML patient samples. The ability to target scaffolding proteins such as beta-arrestin 2 with RNA aptamers may prove beneficial as a therapeutic strategy. Highlights: An RNA aptamer inhibits beta-arrestin 2 activity. Inhibiting beta-arrestin 2 impedes multiple tumorigenic pathways simultaneously. The therapeutic aptamer is delivered to cancer cells using a cell-specific DNA aptamer. Targeting beta-arrestin 2 inhibits tumor progression in CML models and patient samples.
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