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CCAT2 enhances autophagy-related invasion and metastasis via regulating miR-4496 and ELAVL1 in hepatocellular carcinoma |
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| Authors: | Jing Shi Cao Guo Junli Ma |
| Affiliation: | 1. Affiliated Hospital of Jining Medical University, Jining, China Contribution: Data curation (lead), Formal analysis (lead), Methodology (supporting), Project administration (lead), Resources (supporting), Supervision (supporting), Validation (supporting), Visualization (supporting), Writing - original draft (lead);2. Institute of Medical Sciences, Xiangya Hospital, Central South University, Changsha, China Contribution: Data curation (supporting), Formal analysis (supporting), Investigation (equal), Methodology (lead), Project administration (supporting), Software (lead);3. Affiliated Hospital of Jining Medical University, Jining, China |
| Abstract: | 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. |
| Keywords: | autophagy CCAT2 hepatocellular carcinoma metastasis |