Naeem Abdulghani A, Abdulsamad Saud A
Basic Sciences, College of Science and Health Professions, King Saud bin Abdulaziz University for Health Sciences, Jeddah, SAU.
Basic Sciences, King Abdullah International Medical Research Center, Jeddah, SAU.
Cureus. 2025 May 9;17(5):e83813. doi: 10.7759/cureus.83813. eCollection 2025 May.
Prostate cancer is a global health issue and one of the most common reasons for cancer-related mortality. This research aimed to investigate the molecular mechanisms underlying the progression to castration-resistant prostate cancer (CRPC). Differential gene expression was analyzed by contrasting the PNT2 prostate epithelial cell line and the PC3M CRPC cell line. RNA sequencing was performed on three biological replicates of each cell type, and 1,000 differentially expressed genes were identified with a fold change ≥1 and a p<0.05. A heatmap was generated to visualize the gene expression profiles, and the top 10 significantly altered genes were identified. Functional enrichment analysis, including Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis, was conducted to map the biological processes, cellular components, and molecular functions associated with the differentially expressed genes. Furthermore, weighted gene co-expression network analysis was utilized to identify co-expression modules and significant genes, thereby highlighting the top 10 most significant differentially expressed genes in significant pathways. The findings indicate substantial molecular alterations associated with the development of castration-resistant prostate cancer, with major pathways including metabolic deregulation pathways and cell cycle regulation. The identified differentially expressed genes (DEGs) and pathways provide significant insights into disease progression and potential therapeutic targets. These findings contribute to the understanding of prostate cancer at the molecular level and can be used to identify new diagnostic and therapeutic strategies. However, further validation is required to determine the clinical significance of these targets in the treatment of CRPC.
前列腺癌是一个全球性的健康问题，也是癌症相关死亡的最常见原因之一。本研究旨在探讨去势抵抗性前列腺癌（CRPC）进展的分子机制。通过对比PNT2前列腺上皮细胞系和PC3M CRPC细胞系来分析差异基因表达。对每种细胞类型的三个生物学重复样本进行RNA测序，鉴定出1000个差异表达基因，其倍数变化≥1且p<0.05。生成热图以可视化基因表达谱，并确定前10个显著改变的基因。进行了功能富集分析，包括基因本体论和京都基因与基因组百科全书通路分析，以绘制与差异表达基因相关的生物学过程、细胞成分和分子功能。此外，利用加权基因共表达网络分析来识别共表达模块和显著基因，从而突出显著通路中前10个最显著的差异表达基因。研究结果表明，与去势抵抗性前列腺癌的发生发展相关的分子改变很大，主要通路包括代谢失调通路和细胞周期调控。所鉴定的差异表达基因（DEGs）和通路为疾病进展和潜在治疗靶点提供了重要见解。这些发现有助于在分子水平上理解前列腺癌，并可用于识别新的诊断和治疗策略。然而，需要进一步验证以确定这些靶点在CRPC治疗中的临床意义。
