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Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Aberrant adenosine deaminase acting on RNA (ADAR) enzyme activity is associated with aggressive malignancies and poor prognosis.
  • Adenosine-to-inosine (A-to-I) RNA editing is catalyzed by ADAR enzymes, playing a role in various biological processes.
  • The specific role of ADAR in colorectal carcinoma (CRC) and its relationship with the tumor immune microenvironment remain to be fully elucidated.

Purpose of the Study:

  • To investigate the intricate regulatory network of transcript factors and microRNAs involving ADAR in colorectal carcinoma.
  • To explore the association between ADAR gene expression and the immune microenvironment in CRC.
  • To identify ADAR as a potential therapeutic target in colorectal cancer.

Main Methods:

  • Analysis of ADAR mRNA expression, copy number variation, methylation, and mutation status using public databases (cBioPortal, Wanderer, UALCAN).
  • Construction of ADAR-transcript factor and ADAR-microRNA regulatory networks using Cistrome Cancer and miRWalk2.0.
  • Coexpression network analysis (STRING, Cytoscape) and immune cell infiltration analysis (Tumor Immune Estimation Resource, CIBERSORT, GSEA).

Main Results:

  • ADAR mRNA was significantly elevated in colorectal carcinoma and identified as a cancer essential gene.
  • High ADAR mRNA expression correlated with low promoter methylation and high copy number amplification.
  • ADAR coexpression genes were predominantly involved in immunoregulation, particularly T-lymphocyte activation, with enrichment of M1 macrophages and upregulation of hub genes like CD2, CD274, and FASLG in ADAR-high CRC.

Conclusions:

  • ADAR is a crucial gene in colorectal carcinoma, significantly influencing the tumor immune microenvironment.
  • The ADAR-mediated regulatory network plays a key role in immune cell modulation within CRC.
  • ADAR represents a promising novel target for immunotherapy in colorectal cancer.