Differential gene expression analysis after DAPK1 knockout in hepatocellular carcinoma cells

PeerJ. 2022 Aug 2:10:e13711. doi: 10.7717/peerj.13711. eCollection 2022.

Abstract

Background: The mechanism through which death-associated protein kinase 1 (DAPK1) causes hepatocellular carcinoma (HCC) progression remains unclear. In this study, we aimed to identify key proteins that were altered after DAPK1 knockout.

Methods: Stable DAPK1 knockout HCC cell lines were established, then the differentially expressed genes (DEGs) of HCC were screened using the NetworkAnalyst database and enriched using the Metascape software. Protein-protein interaction networks (PPIs) were analyzed and visualized using the STRING database expansion.

Results: In total, 732 differentially expressed genes were identified, including 415 upregulated genes and 317 downregulated genes. Through Cytoscape software scoring, 10 pivotal genes were found to be closely related to changes in DAPK1 expression; Kininogen-1 (KNG1), Complement C3 (C3), Metalloproteinase inhibitor 1 (TIMP1), and Alpha-2-HS-glycoprotein (AHSG) were the most strongly associated with DAPK1 expression changes. Moreover, western blot analysis results revealed that changes in the levels of proteins encoded by the four key genes after DAPK1 knockout were consistent with those seen in the database screening.

Conclusions: These results provide a direction for further studies on the DAPK1 gene and on the mechanism through which DAPK1 leads to hepatocellular carcinoma development.

Keywords: Bioinformatics analysis; DAPK1; Differential gene; Hepatocellular carcinoma; Related gene.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Hepatocellular* / genetics
  • Computational Biology / methods
  • Death-Associated Protein Kinases / genetics
  • Gene Expression Profiling / methods
  • Humans
  • Liver Neoplasms* / genetics
  • Protein Interaction Maps / genetics

Substances

  • DAPK1 protein, human
  • Death-Associated Protein Kinases

Grants and funding

This work was supported by National Natural Science Foudantion of China [81772634]. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.