COL10A1 Facilitates Prostate Cancer Progression by Interacting With INHBA to Activate the PI3K/AKT Pathway.

Prostate cancer (PCa) constitutes a highly common and lethal disease that impacts males globally. However, the specific molecular pathways responsible for its development are still unknown. Therefore, revealing the molecular regulators that contributed to the progression of PCa is pivotal for developing unique management strategies. Through comprehensive bioinformatics analysis of multiple public gene databases, we thoroughly investigated COL10A1 expression level, clinical significance, co-expressed genes and signalling pathways in PCa. COL10A1 and INHBA expression level was assessed in clinical PCa specimens using RT-qPCR, Western blotting and immunohistochemistry. A combination of experimental techniques, including CCK-8 assay, colony formation, flow cytometry, Transwell, wound-healing, immunoprecipitation assays and rescue study, was utilised to examine the fundamental molecular pathways of COL10A1's action across PCa. The COL10A1 expression was significantly elevated in PCa, and its upregulation has been connected with tumour aggressiveness and a weak predictive outcome in subjects. The current investigation revealed that regulation of COL10A1 expression, either by upregulation or downregulation, resulted in sequential augmentation or suppression of PCa cell progression, migration and invasion. Mechanistically, COL10A1 was manifested to directly interact with INHBA and facilitate PI3K and AKT phosphorylation pathways within PCa cells and mouse models. The results of our study offer new perspectives on the tumorigenic role of COL10A1 in PCa and its interactions with INHBA may play important roles in PCa progression.