An oncopeptide regulates m6A recognition by the m6A reader IGF2BP1 and tumorigenesis

Song Zhu, Ji-Zhong Wang, Chen De, Yu-Tian He, Nan Meng, Min Chen, Rui-Xun Lu, Xin-Hui Chen, Xiao-Lan Zhang and Guang-Rong Yan ()
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Song Zhu: The Third Affiliated Hospital of Guangzhou Medical University
Ji-Zhong Wang: The Third Affiliated Hospital of Guangzhou Medical University
Chen De: The Third Affiliated Hospital of Guangzhou Medical University
Yu-Tian He: The Third Affiliated Hospital of Guangzhou Medical University
Nan Meng: The Third Affiliated Hospital of Guangzhou Medical University
Min Chen: The Third Affiliated Hospital of Guangzhou Medical University
Rui-Xun Lu: The Third Affiliated Hospital of Guangzhou Medical University
Xin-Hui Chen: The Third Affiliated Hospital of Guangzhou Medical University
Xiao-Lan Zhang: The Third Affiliated Hospital of Guangzhou Medical University
Guang-Rong Yan: The Third Affiliated Hospital of Guangzhou Medical University

Nature Communications, 2020, vol. 11, issue 1, 1-14

Abstract: Abstract N6-methyladenosine (m6A) is the most prevalent modification in eukaryotic RNAs. The biological importance of m6A relies on m6A readers, which control mRNA fate and function. However, it remains unexplored whether additional regulatory subunits of m6A readers are involved in the m6A recognition on RNAs. Here we discover that the long noncoding RNA (lncRNA) LINC00266-1 encodes a 71-amino acid peptide. The peptide mainly interacts with the RNA-binding proteins, including the m6A reader IGF2BP1, and is thus named “RNA-binding regulatory peptide” (RBRP). RBRP binds to IGF2BP1 and strengthens m6A recognition by IGF2BP1 on RNAs, such as c-Myc mRNA, to increase the mRNA stability and expression of c-Myc, thereby promoting tumorigenesis. Cancer patients with RBRPhigh have a poor prognosis. Thus, the oncopeptide RBRP encoded by LINC00266-1 is a regulatory subunit of m6A readers and strengthens m6A recognition on the target RNAs by the m6A reader to exert its oncogenic functions.

Date: 2020
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DOI: 10.1038/s41467-020-15403-9

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