HOX Genes Linked to Prostate Cancer through Apoptosis, DNA Repair, and Metabolism
Scientists at the University of Surrey have discovered a link between certain HOX genes and prostate cancer, revealing a unique set of genes that are negatively correlated with HOX/PBX inhibitor target gene expression and associated with apoptosis, DNA repair, and metabolism. The study, published in the journal Genes, analyzed publicly available transcriptomic data and found that a specific subgroup of genes shows strong correlations with patient age, reflecting a previously identified progressive loss of regulation of expression in normal peripheral blood cells.
Key Takeaways:
- The study identified a subset of HOX genes that are negatively correlated with HOX/PBX inhibitor target gene expression in prostate cancer.
- These genes are associated with apoptosis, a process of programmed cell death, and are negatively correlated with genes that promote cell adhesion and prevent motility.
- The study found a strong positive correlation between these genes and pathways that support tumour growth, including DNA repair and aminoacyl tRNA biosynthesis.
- The research suggests that these HOX genes may have pro-oncogenic functions in prostate cancer.
- The study used publicly available transcriptomic data and the R2 platform to analyze the expression of HOX genes in prostate cancer cells.
Statistics:
- The study analyzed publicly available transcriptomic data from prostate cancer cells.
- The research found that a specific subgroup of genes is negatively correlated with HOX/PBX inhibitor target gene expression and associated with apoptosis, DNA repair, and metabolism.
- The study found a strong positive correlation between these genes and pathways that support tumour growth, including DNA repair and aminoacyl tRNA biosynthesis.
Sources:
- Genes, 2025;16(7):824.
- Mdpi, St Alban-Anlage 66, Ch-4052 Basel, Switzerland.
- University of Surrey, Faculty of Health and Medical Sciences, Guildford GU2 7XH, UK.
- NewsRx, Health & Medicine Week, August 15, 2025; p 5574.