Abstract:
:The RNA-binding protein (RBP) nucleolin promotes the expression of several proliferative proteins. Nucleolin levels are high in cancer cells, but the mechanisms that control nucleolin expression are unknown. Here, we show that nucleolin abundance is controlled posttranscriptionally via factors that associate with its 3' untranslated region (3'UTR). The RBP HuR was found to interact with the nucleolin (NCL) 3'UTR and specifically promoted nucleolin translation without affecting nucleolin mRNA levels. In human cervical carcinoma HeLa cells, analysis of a traceable NCL 3'UTR bearing MS2 RNA hairpins revealed that NCL RNA was mobilized to processing bodies (PBs) after silencing HuR, suggesting that the repression of nucleolin translation may occur in PBs. Immunoprecipitation of MS2-tagged NCL 3'UTR was used to screen for endogenous repressors of nucleolin synthesis. This search identified miR-494 as a microRNA that potently inhibited nucleolin expression, enhanced NCL mRNA association with argonaute-containing complexes, and induced NCL RNA transport to PBs. Importantly, miR-494 and HuR functionally competed for modulation of nucleolin expression. Moreover, the promotion of cell growth previously attributed to HuR was due in part to the HuR-elicited increase in nucleolin expression. Our collective findings indicate that nucleolin expression is positively regulated by HuR and negatively regulated via competition with miR-494.
journal_name
Mol Cell Bioljournal_title
Molecular and cellular biologyauthors
Tominaga K,Srikantan S,Lee EK,Subaran SS,Martindale JL,Abdelmohsen K,Gorospe Mdoi
10.1128/MCB.05955-11subject
Has Abstractpub_date
2011-10-01 00:00:00pages
4219-31issue
20eissn
0270-7306issn
1098-5549pii
MCB.05955-11journal_volume
31pub_type
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