FKBP10 (FKBP Prolyl Isomerase 10)

FKBP10 is closely linked to tumor progression and treatment response by contributing to metabolic reprogramming, immunosuppressive microenvironment modulation, and programmed cell death regulation, supporting its potential as a biomarker and therapeutic target for predicting prognosis, treatment response, and immunotherapy outcomes.

The risk signature effectively predicts alterations in the tumor immune microenvironment, immunotherapy, chemotherapy sensitivity and intercellular communication across different risk groups. Importantly, our findings reveal that autophagy and liver metastasis synergistically foster an immunosuppressive microenvironment, highlighting a potential target for therapeutic intervention.

Molecular docking revealed strong binding with TLR4 (-9.7 kcal/mol) and TLR9 (-9.4 kcal/mol), and 200 ns molecular dynamics simulations confirmed stable RMSD trajectories, low RMSF at binding residues (<4 Å), persistent hydrogen bonding, compact radius of gyration (38-42 Å for TLR4; ~20 Å for TLR9), favorable total energy (-1400 to -1500 kcal/mol for TLR4; -650 to -720 kcal/mol for TLR9), and stable SASA (~52,000-54,000 Å2). These findings demonstrate that the FKBP10 multi-epitope vaccine is structurally stable, immunogenic, and capable of engaging key innate immune receptors, supporting its potential as a promising immunotherapeutic candidate for synovial sarcoma.

Furthermore, targeting FKBP10 synergized with anti-PD-1 therapy in suppressing tumor growth in vivo. Our work provides a comprehensive molecular atlas of the ccRCC ecosystem, establishes FKBP10 as a key regulator of immune suppression, and highlights its potential as a therapeutic target for personalized immunotherapy.

Clinically, the ITH signature was found to be correlated with a diminished therapeutic efficacy of both conventional transarterial chemoembolization (TACE) and immune checkpoint blockade (ICB). Our study provides a clinically actionable framework for quantifying HCC heterogeneity and reveals ECM remodeling as a potential therapeutic target in high ITH tumors, offering new avenues for personalized treatment strategies.

To the best of our knowledge, this study is the first to demonstrate the integration of S100A8 and Ki67 expression in stromal cells with histological characteristics aids in grading PT.

P=N/A, N=25, Active, not recruiting, Baylor College of Medicine | Trial completion date: Aug 2025 --> Aug 2026

Moreover, by utilizing the CIBERSORT algorithm and immunofluorescence assay, we identified and validated a significant upregulation of M0 macrophages, alongside a downregulation of activated NK cells and CD8+ T cells, which were associated with the presence of LN metastasis in BLCA. Conclusively, these results will provide new insights for future improvements in diagnosis, treatment, and prognosis evaluation for BLCA patients with LN metastasis.

Our mitochondrial-related gene signature, as a risk model, could be a reliable ccRCC prognostic biomarker and could predict the response to immunotherapy. The risk score was correlated with the tumor microenvironment and immune cell infiltration.

Comprehensive characterization of high- and low-risk groups revealed distinct patterns in pathway activation, mutational profiles, immune microenvironment composition, and therapeutic vulnerabilities. Experimental validation confirmed that the key gene FKBP10 promotes malignant phenotypes in tumor cells through IL-6/JAK/STAT3 pathway activation.

FKBP10 overexpression with TP53 mutation predicts poor prognosis and chemoresistance in TNBC. These biomarkers may guide treatment decisions, though prospective validation is needed.