Identification of the shared gene MXD3 signatures and biological mechanism in patients with hip pain and prostate cancer

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Abstract
Prostate cancer (PRAD) is recognized as having a significant effect on systemic illnesses. This study examined possible immune cells, metabolic pathways, and genes that may explain the interaction between PRAD and hip pain. We used information retrieved from the Cancer Genome Atlas and the Gene Expression Omnibus databases. To find common genes, we utilized differential expression analysis and weighted gene co-expression network analysis. The genes that were shared were subjected to pathway enrichment studies using Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes. Additionally, hub genes were analyzed using LASSO regression, and a receiver operating characteristic curve was generated based on the screening outcomes. The genes for the nodes were chosen in a protein–protein interaction network that was built. Single-sample gene-set enrichment analysis was performed to identify the differentially expressed genes. Immunohistochemistry staining confirmed hub gene expression, and single-sample gene-set enrichment analysis assessed immune cell infiltration. We concluded by comparing MAX dimerization protein 3 (MXD3) and MAX interactor 1 (MXI1) expression in tumor tissues using Uniform Manifold Approximation and Projection and violin plots in the Tumor lmmune Single-cell Hub database. After analyzing the intersection of the differentially expressed genes and weighted gene co-expression network analysis-significant module genes, we determined that MXD3 was the best shared diagnostic biomarker for PRAD and hip pain. One potential predictor of PRAD development was the MXI1 node gene, which was found in the protein–protein interaction network. The analyses revealed that MXD3 had a relatively positive correlation with neutrophil and T-helper cell infiltration levels, whereas MXI1 had a negative correlation with mast and Tgd cell levels. Tumors had lower levels of MXI1 expression and higher levels of MXD3 expression compared to normal tissues. Endothelial cells, induced pluripotent stem cells, and smooth muscle cells were all found to express MXI1. This is the first study to investigate the close genetic link between hip pain and PRAD using bioinformatics technologies. The 2 most significant genes involved in crosstalk between PRAD and hip pain were MXD3 and MXI1. The immunological responses triggered by T cells, mast cells, and neutrophils may be crucial in the relationship between PRAD and hip pain.

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