Bioinformatics analysis ofLINC01554and its co-expressed genes in hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related morbidity and mortality globally. Despite the remarkable improvements in comprehensive HCC treatment, the underlying mechanistic details of HCC remain elusive. We screened HCC patients for differentially expressed genes (DEGs) using the Gene Expression Omnibus (GSE113850) and The Cancer Genome Atlas (TCGA) datasets.LINC01554expression in 40 paired samples was determined by quantitative reverse transcription polymerase chain reaction (RT-qPCR), and its clinical significance was assessed.LINC01554was found to have a gain-of-function role in HCCin vitro. Additionally, the bioinformatics analysis of the genes co-expressed withLINC01554was performed using the Co-LncRNA website, and potential molecular mechanisms were investigated using the Gene Ontology and Kyoto Encyclopaedia of Genes and Genomes resources and validated byin vitroexperiments. A total of 229 DEGs were identified from the GSE113850 dataset. Among the identified DEGs, three long non-coding RNAs (lncRNAs) (DIO3OS, LINC01554, andLINC01093) with |logFC| >= 2 and PLINC01554expression levels were significantly correlated with overall survival, pathological stage, hepatitis B infection, tumour size, portal vein tumour thrombus, and TNM stage. Using gain-of-function assays, we further showed thatLINC01554inhibited the proliferation, migration, and invasion of the HCCLM9 and SK-Hep1 cells and promoted G0/G1 arrest, but it did not significantly affect apoptosis. Western blotting revealed thatLINC01554overexpression resulted in increased ZO-1 and E-cadherin expression levels, but decreased N-cadherin and vimentin expression levels. Moreover,LINC01554overexpression inhibited Akt, p-Akt, beta-catenin, and p-Gsk3 beta expression. Our results showed thatLINC01554repressed HCC cell invasiveness and epithelial-to-mesenchymal transition partly by inhibiting Wnt and PI3K-Akt signallingin vitro. Taken together, our findings provide new insights into the molecular mechanisms underlying HCC tumourigenesis and implicateLINC01554as a potential target for HCC therapy.