Long noncoding RNAs have been proved in regulating tumourigenesis, including hepatocellular carcinoma (HCC). However, up to date, the role of PCAT6 in HCC is rare to be reported. In current study, bioinformatics analysis and quantitative realtime PCR were applied to examine the expression of PCAT6 in HCC. The role of PCAT6 in cell proliferation, cell cycle arrest, apoptosis, and metastasis were detected in both gain-and loss-of-function studies by cell biological assays. Bioinformatics analysis was employed to investigate the PCAT6-related genes and pathways in HCC. And we found that PCAT6 was significantly upregulated in HCC tissues and correlated with poor overall survival and disease-free survival in HCC patients. Furthermore, elevated PCAT6 promoted cell proliferation, inhibited cell cycle arrest and cell apoptosis while deficiency of PCAT6 impaired cell proliferation, caused cell cycle arrest and induced cell apoptosis of HCC. Moreover, as for bioinformatics analysis, a total of 389 PCAT6-related genes were found in both HCC tissue and cell lines, and these promising target genes were highly enriched in various key pathways, such as Wnt, HIF-1 signalling pathway, and metabolic pathways. Additionally, among these genes, DCAF13, SNRPB2, RPS8, and FKBP1A were revealed to be overexpressed in HCC and predicted poor prognosis. Taken together, our findings illustrate that PCAT6 contributes to HCC progression and might be a potential target for HCC therapy. Bioinformatics analysis may present a new way for assessing the underlying mechanism of PCAT6 in HCC. Significance of the Study: Hepatocellular carcinoma (HCC) is one of the most common and malignant tumours all over the world. In this study, we observed that PCAT6 was upregulated in HCC and correlated with poor prognosis of HCC patients. PCAT6 could promote cell proliferation, inhibit cell cycle arrest and cell apoptosis of HCC, suggesting PCAT6 exerts tumorigenic role in HCC. Moreover, bioinformatics analysis revealed a total of 389 PCAT6-related genes in both HCC tissue and cell lines, and these promising target genes were highly enriched in various key pathways, such as Yue Luo and Junhao Lin contributed equally to this work.

Long noncoding RNAs (lncRNAs) have been substantially reported to have critical roles in regulating tumorigenesis in recent years. However, the expression pattern and biological function of SNHG17 in hepatocellular carcinoma (HCC) remain unclear. Bioinformatics analysis and qRT-PCR were performed to detect the expression pattern of SNHG17 in HCC tissues, adjacent nontumorous tissues, and cell lines. The effect of SNHG17 on proliferation, migration, and apoptosis of HCC was investigated by knockdown and overexpressing SNHG17 in HCC cell lines. RNA sequencing was utilized to explore the underlying mechanism. Utilizing publicly available TCGA-LIHC, GSE102079 HCC datasets, and qRT-PCR, we found SNHG17 was significantly upregulated in HCC tissues and cell lines and was notably associated with larger tumor size, poorly differentiation, presence of vascular invasion, and advanced TNM stage. Furthermore, gain- and loss-of-function studies demonstrated that SNHG17 promoted cell proliferation and migration and inhibited apoptosis of HCC. By employing RNA sequencing, we found knockdown of SNHG17 caused 1037 differentially expressed genes, highly enriched in several pathways, including metabolic, PI3K-Akt, cell adhesion, regulation of cell proliferation, and apoptotic pathway; among them, 92 were overlapped with SNHG17-related genes in the TCGA-LIHC dataset. Furthermore, ERH, TBCA, TDO2, and PDK4 were successfully validated and found significantly dysregulated in HCC tissues. Moreover, HCC patients with higher SNHG17 expression had a relatively poor overall survival and disease-free survival, and ERH and PDK4 also played a marked role in the prognosis of HCC. Broadly, our findings illustrate that SNHG17 acts as a noncoding oncogene in HCC progression, suggesting its potential value as a novel target for HCC therapy.