THAASHVI BALAJI,DEBALINA SEN,AROCKIA ALEX
DOI: https://doi.org/Prostate cancer (PCa) continues to be a primary cause of cancer-related death in men, with bone metastases being the most prevalent and fatal consequence of advanced illness. This work seeks to clarify the molecular pathways driving prostate cancer growth and its metastatic spread to bone by extensive gene expression profiling and functional analysis of microarray datasets. Differentially expressed genes (DEGs) were found on the GSE69223 (prostate cancer) and GSE14359 (osteosarcoma) datasets using GEO2R and rigorous statistical criteria. A total of 1326 differentially expressed genes (DEGs) were studied in prostate cancer (PCa) and 375 DEGs in osteosarcoma, and the shared genes were used to create a protein-protein interaction (PPI) network with STRING and Cytoscape. Hub genes, including TIMP3, CAV1, ECM1, IGF1, FGF2, and EGF, were recognized as essential contributors to tumor growth. Functional enrichment using Gene Ontology (GO) and KEGG studies indicated severe dysregulation of essential processes, including extracellular matrix (ECM) remodeling, cell adhesion, and signaling pathways such as PI3K-Akt, ECM-receptor interaction, and focal adhesion. Survival research using the UALCAN platform identified IGF1 as a prospective predictive biomarker. These results underscore the pivotal roles of extracellular matrix dynamics, tumor-stroma interactions, and signaling pathways in facilitating metastatic prostate cancer. The discovered genes and pathways provide intriguing candidates for therapeutic intervention and prognostic evaluation, highlighting the potential of transcriptome-based strategies to enhance precision oncology in metastatic prostate cancer.
