LINC02870 facilitates SNAIL translation to promote hepatocellular carcinoma progression

Abstract Exploring the roles of long non-coding RNAs (lncRNAs) in tumorigenesis and metastasis could contribute to recognition of novel diagnostic and therapeutic targets. Herein, we focused on the function and mechanism of LINC02870 in human hepatocellular carcinoma (HCC). We first carried out a pan-cancer study for LINC02870 expression and prognosis, and LINC02870 was determined to be a possible oncogene in HCC. The upregulated expressions of LINC02870 were also found in our HCC samples and more prevalence in the HBV-positive HCC tissues. Moreover, overexpression of LINC02870 promoted cell growth, migration, and invasion in HCC cells. Subsequently, binding proteins of LINC02870 were identified by a number of in silico analyses, including correlation analysis, a signaling network analysis, and survival analysis. Intriguingly, the most promising binding protein of LINC02870 was predicted and confirmed as the eukaryotic translation initiation factor 4 gamma 1 (EIF4G1), an important component of the eukaryotic translation initiation factor 4F (EIF4F) complex to initiate cap-dependent translation. Further investigation presented that LINC02870 increased the translation of SNAIL to induce the malignant phenotypes of HCC cells. Additionally, HCC patients with higher expression levels of LINC02870 and EIF4G1 had a shorter lifespan compared to those with their lower expression levels. Thus, our findings suggested that LINC02870 induced SNAIL translation and correlated with poor prognosis and tumor progression in HBV-related HCC.