术后肝脏再生合成释放的HGF能够改变肿瘤微环境诱导肝癌细胞转移。基于此，体外实验我们利用HGF预先刺激肝癌细胞、体内实验通过裸鼠肝部分切除模型模拟术后微环境改变。我们前期发现HGF刺激肝癌细胞后circERBB3表达显著增多，体外实验表明circERBB3增多促进肝癌细胞侵袭转移。目前circERBB3调控术后肝癌转移作用国内外尚无报道。生物信息学分析及荧光素酶报告实验验证circERBB3通过海绵吸附作用结合miR-20a-5p。生物信息学预测介导线粒体分裂的关键基因DNM1L为miR-20a-5p的下游靶基因。预实验发现HGF刺激后DNM1L表达显著增多，改变circERBB3表达水平引起DNM1L表达相应改变。本研究拟建立circERBB3-miR-20a-5p-DNM1L对话机制，探索circERBB3通过诱导线粒体分裂调控术后肝癌侵袭转移机制，为临床术后早期预防及治疗提供新思路。

HGF released during liver regeneration after surgery can change the tumor microenvironment and induce metastasis of hepatocellular carcinoma (HCC). Based on this, in vitro experiments HGF was used to stimulate HCC cells in advance, and in vivo experiments partial hepatectomy mice models were established to simulate postoperative microenvironment changes. Preliminary experiments found that circERBB3 expression level was significantly increased after HGF stimulating of HCC. And in vitro experiments showed that circERBB3 overexpression promoted invasion and metastasis of HCC. At present, the role of circERBB3 in regulating postoperative HCC metastasis has not been reported. Bioinformatics analysis and luciferase reporter assay confirmed that circERBB3 may function as a sponge for miR-20a-5p. Bioinformatics predicted that DNM1L,a key gene mediating mitochondrial fission, was the downstream target gene of miR-20a-5p.We found that the expression of DNM1L increased significantly after HGF stimulation, and the changes of circERBB3 expression level caused the corresponding changes of DNM1L expression. This study intends to establish a dialogue mechanism of circERBB3-miR-20a-5p-DNM1L and explore the mechanism of circERBB3 regulating postoperative HCC invasion and metastasis by inducing mitochondrial fission. We hope that through this study, to deepen the understanding of new roles of circERBB3 on cancer, and provide new targets for early prevention and early clinical treatment of liver cancer after hepatectomy.