Autophagy is thought to contribute to the pathogenesis of many diseases, including cancer. Long non-coding RNA (lncRNA) CCAT2 functions as an oncogene in a variety of tumours. However, it is still unknown whether CCAT2 is involved in autophagy and metastasis of hepatocellular carcinoma (HCC). In our study, we found that lncRNA CCAT2 expression was significantly increased in HCC tissue and was correlated with advanced stage and venous invasion. Further experiments revealed that CCAT2 induced autophagy and promoted migration and invasion in vitro and in vivo. Mechanistic investigations found that CCAT2 involved in HCC by regulating miR-4496/Atg5 in cytoplasm. In nucleus, CCAT2 bound with ELAVL1/HuR to facilitate HCC progression. Our findings suggest that CCAT2 is an oncogenic factor in the progression of HCC with different regulatory mechanisms and may serve as a target for HCC therapy.

中文翻译：

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CCAT2通过调节miR-4496和ELAVL1增强肝细胞癌中自噬相关的侵袭和转移

自噬被认为有助于许多疾病的发病机制，包括癌症。长链非编码 RNA (lncRNA) CCAT2 在多种肿瘤中作为癌基因发挥作用。然而，CCAT2是否参与肝细胞癌（HCC）的自噬和转移尚不清楚。在我们的研究中，我们发现 lncRNA CCAT2 表达在 HCC 组织中显着增加，并且与晚期和静脉浸润相关。进一步的实验表明，CCAT2在体外和体内诱导自噬并促进迁移和侵袭. 机制研究发现，CCAT2 通过调节细胞质中的 miR-4496/Atg5 参与 HCC。在细胞核中，CCAT2 与 ELAVL1/HuR 结合以促进 HCC 进展。我们的研究结果表明，CCAT2 是 HCC 进展中的致癌因子，具有不同的调节机制，可作为 HCC 治疗的靶点。