LINC00473 mediates cyclin D1 expression through a balance between activation and repression signals in breast cancer cells. Issue 7 (18th March 2019)

• Record Type: Journal Article
• Authors: Shi, Xiangmin; Wang, Xiangting
• Is Part Of: FEBS letters. Volume 593:Issue 7(2019)
• Page Start: 751
• Page End: 759
• Publication Date: 2019-03-18
• Subjects: breast cancer -- CCND1 -- FUS -- LINC00473 -- ncRNACCND1s; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1002/1873-3468.13353
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : Long noncoding RNAs (lncRNAs) are critical regulators in tumorigenesis. However, their roles in breast cancer remain unclear. Here, we found that lncRNA LINC00473 is significantly upregulated in breast cancer cells. Loss‐ or gain‐of‐function experiments show that LINC00473 promotes cell proliferation. Mechanistically, LINC00473 is required for the activation of cyclin D1 (CCND1) expression through recruitment of phosphorylated CREB and histone acetylation to the CCND1 promoter. Interestingly, we found that LINC00473 is also required for maintaining the expression levels of the noncoding RNA CCND1 s and recruiting corepressor FUS to the CCND1 promoter. Altogether, the activation effect of LINC00473 on CCND1 is a net effect of two antagonistic regulatory pathways. Our finding provides a novel lncRNA‐mediated precise transcriptional control of CCND1. Abstract :