SSB cooperates with METTL16-mediated m6A RNA methylation to promote chemoresistance in colorectal cancer cells

Summary: m6A RNA methylation is the most prevalent internal modification in mammalian mRNAs and is involved in many biological processes. METTL16 is a recently identified RNA m6A methyltransferase. However, how METTL16 activity is regulated remains poorly understood. Here, we report a previously unr...

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Bibliografiske detaljer
Main Authors: Haixia Li, Emma Wilkinson, Yan-Hong Cui, Ming Sun, Kenneth Lu, Seungwon Yang, Marc Bissonnette, Yu-Ying He
Format: Article
Sprog:engelsk
Udgivet: Elsevier 2025-07-01
Serier:Cell Reports
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Online adgang:http://www.sciencedirect.com/science/article/pii/S2211124725006977
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Summary:Summary: m6A RNA methylation is the most prevalent internal modification in mammalian mRNAs and is involved in many biological processes. METTL16 is a recently identified RNA m6A methyltransferase. However, how METTL16 activity is regulated remains poorly understood. Here, we report a previously unrecognized mechanism in regulating METTL16 activity. SSB not only serves as a co-factor for METTL16 in installing m6A RNA methylation by enhancing METTL16 binding to RNA but it also is a direct target of METTL16-mediated m6A RNA methylation, leading to a positive auto-regulatory loop that promotes m6A methylation, SSB expression, and chemoresistance in colorectal cancer cells. Our findings reveal the regulation of METTL16 activity by SSB, providing a basis for the development of future therapeutic strategies that target the METTL16/SSB axis in METTL16-dependent cancers such as colorectal cancer.
ISSN:2211-1247