Background: Hepatocellular carcinoma (HCC) is a common malignancy worldwide with a high mortality rate. lncRNA SFTA1P  is highly expressed in HCC. We aimed to study the role of SFTA1P  in HCC and its relationship with miR-4766-5p.
Materials and Methods: The levels of SFTA1P  in HCC tissues and cell lines were determined. Relationship between SFTA1P  and clinical features and prognosis was studied. The influence of SFTA1P  on HCC cell viability, migration, invasion and apoptosis was studied in vitro. Rescue experiments were conducted after the binding site between SFTA1P  and miR-4766-5p confirmed by dual-luciferase assay. The protein expression of AKT, p-AKT, mTOR and p-mTOR in HCC cells with knockdown of SFTA1P  was determined by Western blotting. A tumor study in nude mice was conducted in order to assess the effects of SFTA1P  on tumor growth characteristics.
Results: SFTA1P  was up-regulated in HCC tissues and cell lines. SFTA1P  expression was closely related to tumor size, vascular invasion and TNM stage. Knockdown of SFTA1P  inhibited HCC cell viability, migration and invasion and promoted cell apoptosis. MiR-4766-5p was a target of SFTA1P  and knockdown of SFTA1P  could decrease the protein expression of p-AKT and p-mTOR. Rescue experiments showed that miR-4766-5p mimics could attenuate the promoting role of SFTA1P  on HCC cell viability, invasion and migration, and inhibiting role on cell apoptosis. Moreover, we used nude mice models and also found that the knockdown of SFTA1P  reduced tumor volume and weight.
Conclusion: lncRNA SFTA1P  could promote tumor development in HCC by down-regulating miR-4766-5p expression via PI3K/AKT/mTOR signaling pathway. It may be a potential therapeutic target for HCC.
Keywords: hepatocellular carcinoma, SFTA1P, miR-4766-5p, PI3K/AKT/mTOR signaling pathway, tumor growth