LINC01608 Promotes Hepatocellular Carcinoma Progression Via Regulating MiR-875-5p/EGFR Axis

Objective: Analyze the different expression of LINC01608 in HCC tissues and adjacent normal tissues from TCGA cohort and clinical samples,investigate the role of LINC01608 in HCC malignant effect,and explore the downstream pathway of LINC01608 to explain the molecular mechanism of LINC01608 in regulating HCC progression.Methods: Bioinformatics analyses methods were used to investigate the prognosis of HCC patients among different LINC01608 expression,and the expression of LINC01608 in 60 pairs HCC samples and their matched non-cancerous normal tissues were also measured by quantitative real-time PCR.CCK-8 and colony formation assays were used to demonstrate the effect of LINC01608 on HCC cells proliferation,trans-well and wound-healing assays were used to investigate the role of LINC01608 in HCC cells migration and invasion.The combination of LINC01608 and miR-875-5p were verified by luciferase reporter assays and AGO2 RIP assays.Western blotting assays were used to detect the regulation of EGFR by LINC01608 and miR-875-5p.And xenograft tumor models were used to verify the biological effect of LINC01608 and miR-875-5p in vivo.Results: bioinformatics analyses verified that LINC01608 is overexpressed in HCC tissues and its high expression is associated with poor prognosis.It was also found that LINC01608 promotes HCC cells proliferation,migration,invasion and Epithelial-Mesenchymal Transition(EMT)in vitro and xenograft tumor growth in vivo.Moreover,LINC01608 upregulated EGFR through functioning as a competing endogenous RNA(ce RNA)to sponge miR-875-5p.Finally,reverse experiments showed that restoration of EGFR and inhibition of miR-875-5p could abrogate the effect of LINC01608 silencing.Conclusion: LINC01608/miR-875-5p/EGFR axis were revealed as a novel mechanism in HCC tumorigenesis and progression,which might provide therapeutic strategies for HCC.