IGF2BP3 promotes mRNA degradation through internal m7G modification

Chang Liu, Xiaoyang Dou, Yutao Zhao, Linda Zhang, Lisheng Zhang, Qing Dai, Jun Liu, Tong Wu, Yu Xiao and Chuan He ()
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Chang Liu: The University of Chicago
Xiaoyang Dou: The University of Chicago
Yutao Zhao: The University of Chicago
Linda Zhang: The University of Chicago
Lisheng Zhang: The University of Chicago
Qing Dai: The University of Chicago
Jun Liu: Peking University
Tong Wu: The University of Chicago
Yu Xiao: The University of Chicago
Chuan He: The University of Chicago

Nature Communications, 2024, vol. 15, issue 1, 1-16

Abstract: Abstract Recent studies have suggested that mRNA internal m7G and its writer protein METTL1 are closely related to cell metabolism and cancer regulation. Here, we identify that IGF2BP family proteins IGF2BP1-3 can preferentially bind internal mRNA m7G. Such interactions, especially IGF2BP3 with m7G, could promote the degradation of m7G target transcripts in cancer cells. IGF2BP3 is more responsive to changes of m7G modification, while IGF2BP1 prefers m6A to stabilize the bound transcripts. We also demonstrate that p53 transcript, TP53, is m7G-modified at its 3’UTR in cancer cells. In glioblastoma, the methylation level and the half lifetime of the modified transcript could be modulated by tuning IGF2BP3, or by site-specific targeting of m7G through a dCas13b-guided system, resulting in modulation of cancer progression and chemosensitivity.

Date: 2024
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DOI: 10.1038/s41467-024-51634-w

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