Prostate cancer remains a major medical and social challenge in modern oncology because of its widespread occurrence, high mortality rate among the male population, and substantial impact on demographic health indicators. Based mainly on the assessment of individual genetic factors, existing diagnostic and treatment methods often fail to capture all the complex molecular processes underlying tumor progression. This work implemented an integrative approach that combined bioinformatics and systems biology to construct and comprehensively analyze a protein-protein network derived from 446 pathology-associated genes. Topological analysis of the network revealed key characteristics, including centrality degree and clustering coefficient, and identified 10 key hub genes that are fundamental to the regulation of the cell cycle, apoptotic processes, DNA repair, and oncogenic signaling pathways. Functional annotation demonstrated a strong association of these nodes with the biological processes underlying tumor aggressiveness, therapy resistance, and prognostic potential for individualized disease course prediction. The results not only complement current understandings of the molecular architecture of prostate cancer but also enable the identification of promising biomarkers and potential therapeutic targets, thereby opening new opportunities for experimental validation and clinical application in personalized medicine. This paper underscores the importance of topological analysis for prognostic stratification, optimization of treatment strategies, and guiding new fundamental and applied research in urologic oncology.

Prostate cancer (PCa) remains one of the most prevalent malignancies in men and a leading cause of cancer-related mortality, particularly in its castration-resistant and metastatic forms. Accumulating evidence highlights the central role of cancer stem cells (CSCs) in tumor initiation, progression, intratumoral heterogeneity, and the resistance to therapy and radiation. This review summarizes current data and provides an in-depth analysis of four promossing regulators of CSC-associated stemness and cellular plasticity: the oncoprotein MUC1-C, the type II transmembrane serine protease TMPRSS4, the orphan nuclear receptor TLX, and the PDZ-domain adaptor protein MDA-9/Syntenin. For each molecule, we discuss structural features, expression patterns in prostate tissue, and involvement in key oncogenic signaling pathways, including Wnt/β-catenin, PI3K/AKT, MAPK, STAT3, NOTCH, and TGF-β. Their contributions to epithelial-mesenchymal transition (EMT), maintenance of the CSC phenotype, androgen-independent growth, and resistance to standard therapies are examined in detail. Particular emphasis is placed on in vitro and in vivo evidence demonstrating the significance of MUC1-C, TMPRSS4, TLX, and MDA-9/syntenin as biomarkers of aggressive PCa and as targets for precision therapeutics and immunotherapy.