Bioinformatics analysis of LINC01554 and its co‑expressed genes in hepatocellular carcinoma

Abstract

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. LINC01554 expression in 40 paired samples was determined by quantitative reverse transcription polymerase chain reaction (RT-qPCR), and its clinical significance was assessed. LINC01554 was found to have a gain-of-function role in HCC in vitro. Additionally, the bioinformatics analysis of the genes co-expressed with LINC01554 was 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 by in vitro experiments. A total of 229 DEGs were identified from the GSE113850 dataset. Among the identified DEGs, three long non-coding RNAs (lncRNAs) (DIO3OS, LINC01554, and LINC01093) with |logFC| ≥2 and P<0.05 were screened. A total of 148 lncRNAs with |logFC| ≥1 and P<0.05 were identified from TCGA dataset. Low LINC01554 expression 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 that LINC01554 inhibited 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 that LINC01554 overexpression resulted in increased ZO-1 and E-cadherin expression levels, but decreased N-cadherin and vimentin expression levels. Moreover, LINC01554 overexpression inhibited Akt, p-Akt, β-catenin, and p-Gsk3β expression. Our results showed that LINC01554 repressed HCC cell invasiveness and epithelial-to-mesenchymal transition partly by inhibiting Wnt and PI3K-Akt signalling in vitro. Taken together, our findings provide new insights into the molecular mechanisms underlying HCC tumourigenesis and implicate LINC01554 as a potential target for HCC therapy.

Long Noncoding RNA LINC01554 Inhibits the Progression of NSCLC Progression by Functioning as a ceRNA for miR-1267 and Regulating ING3/Akt/mTOR Pathway

“…In our study, results showed that NSCLC cell proliferation could be inhibited by overexpressed LINC01554 both in vivo and in vitro. The above results were in accordance with the previous study [2,12,19,20], which indicated that LINC01554 played a tumour suppressive role in NSCLC development.…”

Single-Cell Sequencing of Hepatocellular Carcinoma Reveals Cell Interactions and Cell Heterogeneity in the Microenvironment

“… 26 , 27 It has been reported that low expression of LINC01554 is significantly correlated with overall survival, pathological stage, hepatitis B infection, tumor size, portal vein tumor thrombus and TNM stage. 28 This is consistent with our finding that low expression of LINC01554 indicates a poor prognosis.…”

Identifying Prognostic Significance of RCL1 and Four-Gene Signature as Novel Potential Biomarkers in HCC Patients

“…In this study, three survivalrelated LncRNAs, AC079061, AL354872, and LINC01093, were identified, and these LncRNAs had a strong correlation with RCL1 expression. LINC01093 has been shown to be significantly downregulated in HCC and was correlated with tumor cell proliferation and metastasis [31][32][33]. However, the function of AC079061 and AL354872 in HCC remained unclear.…”