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C/EBPβ contributes to transcriptional activation of long non-coding RNA NEAT1 during APL cell differentiation
- Wang, Yewei, Fu, Lei, Sun, Ailian, Tang, Doudou, Xu, Yunxiao, Li, Zheyuan, Chen, Mingjie, Zhang, Guangsen
- Biochemical and biophysical research communications 2018 v.499 no.2 pp. 99-104
- binding sites, carcinogenesis, cell differentiation, chromatin, leukemia, luciferase, non-coding RNA, precipitin tests, retinoic acid, therapeutics, transcription factors, transcriptional activation
- Emerging evidences have shown that long non-coding RNAs (lncRNAs) play critical roles in cancer development and cancer therapy. LncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) is indispensable during acute promyelocytic leukemia (APL) cell differentiation induced by all-trans retinoic acid (ATRA). However, the precise mechanism of NEAT1 upregulation has not been fully understood. In this study, we performed chromatin immunoprecipitation and luciferase reporter assays to demonstrate that C/EBP family transcription factor C/EBPβ bind to and transactivate the promoter of lncRNA NEAT1 through the C/EBPβ binding sites both around −54 bp and −1453 bp upstream of the transcription start site. Moreover, the expression of C/EBPβ was increased after ATRA treatment, and the binding of C/EBPβ in the NEAT1 promoter was also dramatically increased. Finally, knockdown of C/EBPβ significantly reduced the ATRA-induced upregulation of NEAT1. In conclusion, C/EBPβ directly activates the expression of NEAT1 through binding to the promoter of NEAT1. Knockdown of C/EBPβ impairs ATRA-induced transcriptional activation of NEAT1. Our data indicate that C/EBPβ contributes to ATRA-induced activation of NEAT1 during APL cell differentiation. Our results enrich our knowledge on the regulation of lncRNAs and the regulatory role of C/EBPβ in APL cell differentiation.