The SNHG1-Centered ceRNA Network Regulates Cell Cycle and Is a Potential Prognostic Biomarker for Hepatocellular Carcinoma

Abstract

Hepatocellular carcinoma (HCC) is one of the most common and lethal types of cancer. This study aimed to identify the expression regulatory network and a prognostic signature of HCC.RNA-seq data from The Cancer Genome Atlas were used to identify the differentially expressed genes (DEGs) between HCC and normal liver tissues. DEGs were subjected to the construction of protein-protein interaction (PPI) network and enrichment analysis of Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways. The results showed that most of the DEGs were enriched in the cell cycle pathway, and the top 10 hub genes in the PPI network belong to the cell cycle pathway. A ceRNA network was constructed using starBase database, including one lncRNA (SNHG1), seven miRNAs (miR-195-5p, miR-199a-3p, miR-199a-5p, miR-199b-3p, miR-383-5p, miR-424-5p and miR-654-3p) and six of the top 10 hub genes (BUB1,CCNA2, CCNB1, KIF11, NCAPG, and TOP2A).In vitro experiments showed that knockdown of SNHG1 in the HCC cell lines (Huh7 and HepG2) decreased the expression of the six hub genes and cell viability, leading to cell cycle arrest at the G1 phase. These findings indicate that SNHG1 promotes cell proliferation by regulating cell cycle-related genes as a ceRNA. Additionally, Kaplan-Meier's survival and multivariate Cox regression analysis identified a prognostic signature of seven genes (including SNHG1 and the six SNHG1-regulated hub genes) for overall survival (OS) of HCC patients. In conclusion, this study identified a novel regulatory network in HCC and a potential independent prognostic factor for OS of HCC patients.

Diabetes and diabetic associative diseases: An overview of epigenetic regulations of TUG1

“…Overexpressing TUG1 promoted TIMP3 expression by targeting miR-21, reducing cell and renal fibrosis. These findings suggest that TUG1 indirectly regulates TIMP3 via miR-21, potentially offering a strategy to mitigate DN-related fibrosis ( Wang et al, 2019 , Zhou et al, 2022a , Zhou et al, 2022b , Zhou et al, 2022c ).…”

“…With links also expression MALAT1 ER stress 'with links also expression MALAT1′ markers. TUG1 and MEG3 might serve as markers for identifying ER stress associated with hyperglycemia in diabetes ( Zhou et al, 2022a , Zhou et al, 2022b , Zhou et al, 2022c , Heydari et al, 2023 ). PDGF-BB/Wnt signaling, a vital pathway, plays a significant role in diabetes.…”

“…This improvement was associated with enhanced mitochondrial function in podocytes. It has been demonstrated that Tug1 and PGC-1α interaction enhances PGC-1α adherence to its supporter, highlighting their role in adjusting the bioenergetics of the mitochondria in the diabetes environment ( Long et al, 2016 , Zhou et al, 2022a , Zhou et al, 2022b , Zhou et al, 2022c ). Tissue inhibitor of metalloproteinase 3 (TIMP3) is a protein that regulates extracellular matrix remodelling by inhibiting MMPs.…”

Autophagy‐associated non‐coding RNAs: Unraveling their impact on Parkinson's disease pathogenesis

“…82,83 3.1.1 | MiRNAs' role in neuroprotection through autophagy modulation miRNAs are being shown to be involved in the pathogenic mechanism of PD by triggering autophagy. [82][83][84] For example, the level of miR-326 reduces when PINK1, a gene associated with PD, is not present. 82 Injecting a miR-326 replica into mice injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) reduces the amounts of α-syn and stimulated nitric oxide (NO) synthase and alleviates the movement difficulties of the animals by enhancing the breakdown of DopNs via triggering of JNK network by blocking XBP1.…”

“…miRNAs are being shown to be involved in the pathogenic mechanism of PD by triggering autophagy 82–84 . For example, the level of miR‐326 reduces when PINK1, a gene associated with PD, is not present 82 .…”