AI Article Synopsis
- The study investigates the role of ACKR2, a chemokine scavenger, in relation to cancer prognosis, focusing on its genetic and epigenetic regulation.
- Data from major cancer databases revealed that higher levels of ACKR2 are linked to better survival outcomes in uveal melanoma and liver hepatocellular carcinoma, and its expression is influenced by various factors such as gene copy number and mutations.
- The findings suggest that changes in ACKR2 levels can serve as potential biomarkers for cancer prognosis and are connected to alterations in specific genes involved in RNA modifications.
Article Abstract
Objective: ACKR2 is a scavenger for most inflammation-related CC chemokines. This study aimed to assess the pan-cancer prognostic significance of ACKR2 and the genetic and epigenetic mechanisms underlying its dysregulation.
Methods: Pan-cancer data from The Cancer Genome Atlas (TCGA), Therapeutically Applicable Research to Generate Effective Treatments (TARGET) and The Genotype-Tissue Expression (GTEx) were integrated and analyzed.
Results: ACKR2 is consistently associated with favorable progression-free interval (PFI) and overall survival (OS) in TCGA-uveal melanoma (UVM) and TCGA-liver hepatocellular carcinoma (LIHC). ACKR2 is negatively correlated with the expression of CCL1, CCL4, CCL5, CXCL8, CCL17, and CCL20 in TCGA-UVM and TCGA-LIHC. The group with gene copy gain had significantly higher ACKR2 expression than those with loss. The lower ACKR2 expression groups were associated with a significantly higher ratio of BAP1 mutations. In addition, ACKR2 was negatively corrected with DNMT1 expression but was positively corrected with ZC3H13, an m6A writer gene and NSUN3, an RNA m5C writer gene.
Conclusions: ACKR2 expression was associated with favorable prognosis in patients with uveal melanoma and hepatocellular carcinoma. ACKR2 dysregulation might be an accumulated result of gene copy number alterations, transcriptional disruption, and RNA modifications.
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| http://dx.doi.org/10.1080/1744666X.2023.2274361 | DOI Listing |
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