Introduction: Hepatocellular carcinoma (HCC), a prevalent and aggressive form of cancer, poses significant challenges due to its limited therapeutic options. This study aims to leverage multi-omics data from liver cancer to identify potential therapeutic targets for HCC. Methods: We employed an integrative approach by analyzing various omics datasets related to liver cancer. Through comprehensive data mining and analysis, we identified key genes that are significantly associated with HCC. To gain insights into their biological roles and underlying mechanisms, we constructed gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway networks. Specifically, we focused on genes that exhibited high expression levels in HCC and were correlated with poor patient prognosis. Among these, CDK1 and DLGAP5 emerged as promising candidates and were further investigated for their potential involvement in tumor immune cell infiltration and HCC progression. Results: Our analysis revealed that CDK1 and DLGAP5 are highly expressed in HCC tissues compared to normal liver tissues, and their elevated expression is associated with unfavorable clinical outcomes. Furthermore, through GO and KEGG pathway analyses, we found that these genes are implicated in critical biological processes and signaling pathways relevant to HCC pathogenesis. Notably, CDK1 and DLGAP5 were shown to be associated with tumor immune cell infiltration, suggesting their potential role in modulating the tumor microenvironment and promoting HCC progression. Discussion: These findings provide valuable insights into the development of novel therapeutic approaches for HCC.

Background: S100 calcium-binding protein A6 (S100A6) is a calcium-binding protein that is involved in a variety of cellular processes, such as proliferation, apoptosis, and the cellular response to various stress stimuli. However, its role in NAFLD and associated metabolic diseases remains uncertain. Methods and Results: In this study, we revealed a new function and mechanism of S100A6 in NAFLD. S100A6 expression was upregulated in human and mouse livers with hepatic steatosis, and the depletion of hepatic S100A6 remarkably inhibited lipid accumulation, insulin resistance, inflammation, and obesity in a high-fat, high-cholesterol (HFHC) diet-induced murine hepatic steatosis model. In vitro mechanistic investigations showed that the depletion of S100A6 in hepatocytes restored lipophagy, suggesting S100A6 inhibition could alleviate HFHC-induced NAFLD. Moreover, S100A6 liver-specific ablation mediated by AAV9 alleviated NAFLD in obese mice. Conclusions: Our study demonstrates that S100A6 functions as a positive regulator of NAFLD, targeting the S100A6-lipophagy axis may be a promising treatment option for NAFLD and associated metabolic diseases. Export

Hepatocellular carcinoma (HCC) is a prevalent and aggressive malignancy with limited treatment options. Therefore, the identification of novel drug candidate target genes is crucial for the development of effective therapeutic strategies for HCC. In this study, we employed deeply bioinformatics analysis to identify potential therapeutic targets for HCC. Key genes were identified in HCC, and gene ontology (GO) and KEGG pathway networks were constructed to explore their biological functions and associated pathways. CDK1 and DLGAP5 were highly expressed in HCC and associated with poor prognosis. Additionally, CDK1 and DLGAP5 were found to be associated with tumor immune cell infiltration to promote HCC. These findings provide valuable insights into the development of novel therapeutic approaches for HCC.