Objective: Herein, we aimed at exploring the FAP expression in clear cell renal cell carcinoma (ccRCC) along with its clinical implication.Methods: Using computational tools analysis of different freely accessible gene databases, the expression pattern, clinical importance, co-expressed genes, and signaling pathways of FAP in ccRCC were thoroughly investigated. FAP expression was examined in clinical ccRCC specimens through qRT-PCR, western blotting and immunohistochemistry. Furthermore, in vitro and in vivo experiments were carried out using flow cytometry, CCK-8, wound-healing and Transwell assays, as well as xenograft tumor model, respectively.Results: FAP levels were found to be significantly elevated in ccRCC based on bioinformatic data from public databases. Patients who exhibited higher expression levels of FAP had poorer prognoses, according to Kaplan–Meier analysis of survival data. In addition, diagnostic and prognostic value of FAP in ccRCC was figured out by ROC curve and prognostic nomogram model. In vitro study revealed that the over-expression FAP accelerated cell proliferation, migration as well as invasion, and suppressed cell apoptosis, but silencing of FAP had the opposite effect. FAP suppression reduced the PI3K/AKT/mTOR pathway's stimulation, whereas FAP up-regulation increased the stimulation of the pathway. Blocking the PI3K/AKT/mTOR signaling pathway with the dual PI3K/mTOR inhibitor BEZ235 repressesed cancer-promoting effect of FAP. Additionally, we found that the downregulation of FAP was effective at slowing tumor progression in vivo.Conclusion: It is possible that FAP could be a reliable biomarker for the diagnosis and prognosis of ccRCC because of its role in the ccRCC progression via triggering the PI3K/AKT/mTOR signaling 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.