Cancer cell growth suppression by a 62nt AU-rich RNA from C/EBPβ 3′UTR through competitive binding with HuR

• Published in: Biochemical and biophysical research communications 2012-09, Vol.426 (1), p.122-128
• Main Authors: Sun, Da-Quan, Wang, Ying, Liu, Ding-Gan
• Format: Article
• Language: English
• Subjects: AU Rich Elements; Base Sequence; Binding, Competitive; C/EBPβ 3′UTR; CCAAT-Enhancer-Binding Protein-beta - genetics; Cell Line, Tumor; Cell Proliferation; Competitive binding; Distinct AU-rich RNA; ELAV Proteins - metabolism; Humans; HuR; Liver Neoplasms - pathology; Molecular Sequence Data; Tumor suppression
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2012.08.049

► A 62nt RNA with AU-rich regions was isolated from the C/EBPβ 3′UTR. ► This 62nt RNA (R62) was introduced into a human hepatocarcinoma cell line. ► R62 suppressed cell growth rate and induced apoptosis. ► R62 specifically bound HuR. ► R62 competed with C/EBPβ mRNA for binding HuR. AU-rich elements are functional motifs in the 3′untranslated region of mRNA and are binding sites for the RNA binding protein HuR, an mRNA stabilizer and translation enhancer implicated in carcinogenesis. It is not clear whether, and, if so, how the AU-rich elements function in cells when they are separated from their mRNA and form an independent RNA species. Here, we show that a short RNA with AU-rich elements derived from C/EBPβ 3′UTR suppressed growth in a human liver cancer cell line. It specifically bound HuR, and it competed with C/EBPβ mRNA in order to bind to HuR. Our results provide evidence that the cancer cell growth suppression by this 62nt RNA containing AU-rich elements may be due to competitive binding to HuR. This work may open new options for the development of novel anti-cancer drugs.