The alternative spliced 3'-UTR mediated differential secretion of macrophage colony stimulating factor in breast cancer cells.
AffiliationUniv Arizona, Canc Ctr
Univ Arizona, Dept Obstet & Gynecol
MetadataShow full item record
PublisherACADEMIC PRESS INC ELSEVIER SCIENCE
CitationWoo, H. H., & Chambers, S. K. (2020). The alternative spliced 3′-UTR mediated differential secretion of macrophage colony stimulating factor in breast cancer cells. Biochemical and Biophysical Research Communications.
Rights© 2020 Published by Elsevier Inc.
Collection InformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at email@example.com.
AbstractCSF-1 mRNA 3'UTR variants (var) are generated from alternative splicing. CSF-1 protein encoded by var-1 mRNA with long 3'UTR derived from exon-10 is rapidly secreted compared to the CSF-1 protein encoded by var-4 mRNA with short 3'UTR derived from exon-9. Secretion kinetics indicates that HuR, which binds the CSF-1 var-1 mRNA, but not var-4 mRNA, accelerates the secretion of CSF-1 protein. HuR over-expression increases the secretion rate of CSF-1 protein. In contrast, silencing of HuR does not have such an effect, suggesting other compensatory mechanisms. Effect of the CSF-1 mRNA variant 3'UTRs on cellular phenotype shows both CSF-1 var-1 or -4 mRNA is involved in the enhanced rates of migration and invasion observed by both in vitro in breast cancer cells. Our study indicates that the alternative splicing of CSF-1 mRNA 3'UTR can regulate differential secretion of CSF-1 protein. (C) 2020 Published by Elsevier Inc.
Note12 month embargo; available online 13 March 2020
VersionFinal accepted manuscript
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