N-methyladenosine (mA) is the most common RNA modification in eukaryotic RNAs. Although the important roles of mA in RNA fate have been revealed, the potential contribution of mA to RNA function in various diseases, including hepatocellular carcinoma (HCC), is still unclear. In this study, we identified a novel mA-modified RNA AC026356.1. We found that AC026356.1 was increased in HCC tissues and cell lines. High expression of AC026356.1 was correlated with poor survival of HCC patients. mA modification level of AC026356.1 was also increased in HCC and more significantly correlated with poor survival of HCC patients. Functional assays showed that mA-modified AC026356.1 promoted HCC cellular proliferation, migration, and liver metastasis. Gene set enrichment analysis showed that AC026356.1 activated IL11/STAT3 signaling. Mechanistic investigation showed that mA-modified AC026356.1 bound to IGF2BP1. The interaction between mA-modified AC026356.1 and IGF2BP1 promoted the binding of IL11 mRNA to IGF2BP1, leading to increased IL11 mRNA stability and IL11 secretion. Functional rescue assays showed that depletion of IL11 reversed the oncogenic roles of AC026356.1. These findings revealed the potential influences of mA modification on RNA biological functions and suggested that targeting mA modification may be a novel strategy for HCC treatment.
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| http://dx.doi.org/10.1038/s41598-023-45449-w | DOI Listing |
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