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Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. Increasing evidences have demonstrated that ILF3 antisense RNA 1 (ILF3-AS1) acts as an oncogenic long noncoding RNA (lncRNA) in… Click to show full abstract
Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. Increasing evidences have demonstrated that ILF3 antisense RNA 1 (ILF3-AS1) acts as an oncogenic long noncoding RNA (lncRNA) in several types of human cancers. However, the expression pattern, functional role and underlying mechanism of ILF3-AS1 in HCC remains largely unclear. Here, we found that ILF3-AS1 expression was significantly elevated in HCC tissues and also associated with prognosis of patients with HCC. Functional assays demonstrated that knockdown of ILF3-AS1 expression resulted in the suppression of proliferation, migration and invasion in HCC cells, whereas overexpression of ILF3-AS1 exerted opposite effects. Additionally, knockdown of IFL3-AS1 attenuated HCC tumorigenesis and metastasis in vivo. Mechanistically, ILF3-AS1 associated with ILF3 mRNA and inhibited its degradation. ILF3-AS1 increased ILF3 m6A level via recruiting N6-methyladenosine (m6A) RNA methyltransferase METTL3. Moreover, IFL3-AS1 enhanced the interaction between ILF3 mRNA and m6A reader IGF2BP1. Overall, our study revealed the function and mechanism of ILF3-AS1 in the malignant phenotypes of HCC cells, which provides a novel therapeutic target for HCC.