Long non-coding RNA UCA1 promotes breast tumor growth by suppression of p27 (Kip1).

摘要: Functional genomics studies have led to the discovery of a large amount non-coding RNAs from human genome; among them are long (lncRNAs). Emerging evidence indicates that lncRNAs could critical role in regulation cellular processes such as cell growth and apoptosis well cancer progression metastasis. As master gene regulators, capable forming lncRNA–protein (ribonucleoprotein) complexes regulate number genes. For example, lincRNA-RoR suppresses p53 response DNA damage through interaction with heterogeneous nuclear ribonucleoprotein I (hnRNP I). The present study demonstrates hnRNP can also form functional complex lncRNA urothelial carcinoma-associated 1 (UCA1) increase UCA1 stability. Of interest, phosphorylated I, predominantly cytoplasm, is responsible for UCA1. Moreover, although enhances translation p27 (Kip1) 5′-untranslated region (5′-UTR) mRNAs, protein level by competitive inhibition. In support this finding, has an oncogenic breast both vitro vivo. Finally, we show negative correlation between UCA tumor tissue microarray. Together, our results suggest important cancer.