前期我们采用全转录组测序，发现LVCAT-7在肝癌高于癌旁正常肝组织；体外实验表明：LVACT-7促进肝癌细胞侵袭迁移,且与miR-195-5p、miR-203a-3p.1负相关；LVCAT-7竞争性结合miR-195-5p和miR-203a-3p.1，调控ROCK1和DKK2蛋白表达。为验证肝癌LVCAT-7增高，同时结合miR-195-5p和miR-203a-3p.1，分别导致下游靶蛋白ROCK1和DKK2升高，两条途径均能促进肝癌侵袭转移。拟开展①肝癌临床分期与LVCAT-7、miR-195-5p、miR-203a-3p.1、ROCK1、DKK2的关系；②运用qPCR、荧光素酶报告、RIP、pull down等实验，明确LVCAT-7作为ceRNA，介导miRNA-195-5p/ROCK1和miRNA-203a-3p.1/DKK2的表达，促进肝癌侵袭转移，为肝癌诊断和治疗开辟新领域。

In the previous studies, we found that LVCAT-7 was higher expression in HCC compare with adjacent tissue by RNA-seq. Our studies further showed that the higher invasion and migration of HCC cells were promoted by LVACT-7, which was negatively correlated with miR-195-5p and miR-203a-3p.1. LVCAT-7 indirectly regulate the expression of ROCK1 and DKK2 proteins via competitive combination with miR-195-5p and miR-203a-3p.1. Here, we propose hypothesis that the increase of LVCAT-7 in HCC contains sites to bind with miR-195-5p and miR-203a-3p.1, to upregulate the expression of the downstream target protein ROCK1 and DKK2 respectively. Both of them can promote the invasion and metastasis of HCC. Consequently, we plan to carry out the clinical research to reveal the relationships among HCC, LVCAT-7, miR-195-5p, miR-203a-3p.1, ROCK1, DKK2. in addition, to confirm the expression of miRNA-195-5p/ROCK1 and miRNA-203a-3p.1/DKK2 was mediated by LVCAT-7 as ceRNA to promote the invasion and metastasis of HCC by performing qPCR, luciferase report, RIP, pull down and other experimental methods. our study may serve as a new diagnostic marker or target for treatment of HCC patients.