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LINC00473 mediates cyclin D1 expression through a balance between activation and repression signals in breast cancer cells
Author(s) -
Shi Xiangmin,
Wang Xiangting
Publication year - 2019
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.13353
Subject(s) - corepressor , cyclin d1 , cancer research , psychological repression , breast cancer , carcinogenesis , histone , regulation of gene expression , cancer , gene expression , microbiology and biotechnology , biology , cell cycle , chemistry , gene , genetics
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.