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.

肝细胞癌（HCC）是全球最常见的恶性肿瘤之一。越来越多的证据表明，ILF3 反义 RNA 1 (ILF3-AS1) 在多种人类癌症中充当致癌长非编码 RNA (lncRNA)。然而，ILF3-AS1 在 HCC 中的表达模式、功能作用和潜在机制仍不清楚。在这里，我们发现 ILF3-AS1 表达在 HCC 组织中显着升高，并且还与 HCC 患者的预后相关。功能测定表明，ILF3-AS1 表达的敲低导致 HCC 细胞增殖、迁移和侵袭的抑制，而 ILF3-AS1 的过表达则发挥相反的作用。此外，IFL3-AS1 的敲低减弱了体内 HCC 肿瘤发生和转移。机械地，ILF3-AS1 与 ILF3 mRNA 相关并抑制其降解。ILF3-AS1 增加 ILF3 m通过募集 N ⁶ -甲基腺苷(m ⁶ A) RNA 甲基转移酶 METTL3 达到^{6 A 水平。}此外，IFL3-AS1 增强了 ILF3 mRNA 和 m ⁶ A reader IGF2BP1 之间的相互作用。总体而言，我们的研究揭示了ILF3-AS1在HCC细胞恶性表型中的作用和机制，为HCC提供了新的治疗靶点。