Abstract
Background: Nonalcoholic fatty liver disease (NAFLD) is now recognized as the most prevalent chronic liver disease worldwide. However, the dysregulated gene expression for NAFLD is still poorly understood. Material and methods: We analyzed two public datasets (GSE48452 and GSE89632) to identify differentially expressed genes (DEGs) in NAFLD. Then, we performed a series of bioinformatics analyses to explore potential hub genes in NAFLD. Results: This study included 26 simple steatosis (SS), 34 nonalcoholic steatohepatitis (NASH), and 13 healthy controls (HC). We observed 6 up- and 19 down-regulated genes in SS, and 13 up- and 19 down-regulated genes in NASH compared with HC. Meanwhile, the overlapping pathways between SS and NASH were PI3K-Akt signaling pathway and pathways in cancer. Then, we screened out 10 hub genes by weighted Gene Co-Expression Network Analysis (WGCNA) and protein-protein interaction (PPI) networks. Eventually, we found that CYP7A1/GINS2/PDLIM3 were associated with the prognosis of hepatocellular carcinoma (HCC) in the TCGA database. Conclusion: Although further validation is still needed, we provide useful and novel information to explore the potential candidate genes for NAFLD prognosis and therapeutic options.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is recognized as the most prevalent chronic liver disease worldwide, with a prevalence ranging from 13% in Africa to 42% in southeast Asia, and it may become the major cause of end-stage liver diseases by 2025 (Zarrinpar et al, 2016; Younossi, 2019; Huang et al, 2021)
We found 13 up- and 19 down-regulated genes in nonalcoholic steatohepatitis (NASH) compared with healthy controls (HC) (Figure 2D)
We found that CYP7A1, GINS2, and PDLIM3 were significantly up-regulated, and MYC, MAMDC4, ADAMTS1, THBS1, and RASD1 were significantly down-regulated in hepatocellular carcinoma (HCC) tumor samples compared with normal samples using the The Cancer Genome Atlas (TCGA) dataset (Figure 6A)
Summary
Nonalcoholic fatty liver disease (NAFLD) is recognized as the most prevalent chronic liver disease worldwide, with a prevalence ranging from 13% in Africa to 42% in southeast Asia, and it may become the major cause of end-stage liver diseases by 2025 (Zarrinpar et al, 2016; Younossi, 2019; Huang et al, 2021). NAFLD represents a spectrum of disease severity, ranging from simple steatosis (SS) termed as nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC) (Natarajan et al, 2014). It has been well-recognized that obesity, insulin resistance, and type 2 diabetes mellitus are the strongest risk factors for NAFLD (Chen and Tian, 2020). The dysregulated gene expression for NAFLD is still poorly understood
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