We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
A peptide encoded by circular form of LINC-PINT suppresses oncogenic transcriptional elongation in glioblastoma.
- Authors
Zhang, Maolei; Zhao, Kun; Xu, Xiaoping; Yang, Yibing; Yan, Sheng; Wei, Ping; Liu, Hui; Xu, Jianbo; Xiao, Feizhe; Zhou, Huangkai; Yang, Xuesong; Huang, Nunu; Liu, Jinglei; He, Kejun; Xie, Keping; Zhang, Gong; Huang, Suyun; Zhang, Nu
- Abstract
Circular RNAs (circRNAs) are a large class of transcripts in the mammalian genome. Although the translation of circRNAs was reported, additional coding circRNAs and the functions of their translated products remain elusive. Here, we demonstrate that an endogenous circRNA generated from a long noncoding RNA encodes regulatory peptides. Through ribosome nascent-chain complex-bound RNA sequencing (RNC-seq), we discover several peptides potentially encoded by circRNAs. We identify an 87-amino-acid peptide encoded by the circular form of the long intergenic non-protein-coding RNA p53-induced transcript (LINC-PINT) that suppresses glioblastoma cell proliferation in vitro and in vivo. This peptide directly interacts with polymerase associated factor complex (PAF1c) and inhibits the transcriptional elongation of multiple oncogenes. The expression of this peptide and its corresponding circRNA are decreased in glioblastoma compared with the levels in normal tissues. Our results establish the existence of peptides encoded by circRNAs and demonstrate their potential functions in glioblastoma tumorigenesis. Functional peptides can be encoded by short open reading frames in non-coding RNA. Here, the authors identify a 87aa peptide encoded by the circular form of the long intergenic non-protein-coding RNA p53-induced transcript (LINC-PINT) that can reduce glioblastoma proliferation via interaction with PAF1 which sequentially inhibits the transcriptional elongation of some oncogenes.
- Publication
Nature Communications, 2018, Vol 9, p1
- ISSN
2041-1723
- Publication type
Article
- DOI
10.1038/s41467-018-06862-2