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ARTICLE

Integrative Multi-Omics and Single-Cell Analyses Identify FKBP10 as a CAF-Associated Biomarker Linked to ECM Remodeling and Aggressiveness in Neuroblastoma

Zhaolong Wang#, Baocheng Gong#, Chaoyu Wang#, Zhongyuan Li, Shuai Man, Na Lei, Jiarun Fu, Yan Jin*, Benfu Zhong*, Qiang Zhao*
Department of Pediatric Oncology, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for Cancer, Tianjin’s Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China
* Corresponding Author: Yan Jin. Email: email; Benfu Zhong. Email: email; Qiang Zhao. Email: email
# These authors contributed equally to this work

Oncology Research https://doi.org/10.32604/or.2026.087891

Received 24 June 2026; Accepted 10 September 2026; Published online 20 September 2026

Abstract

Objectives: Neuroblastoma (NB) is a heterogeneous pediatric malignancy driven by both intrinsic oncogenic programs and the stromal microenvironment. However, the critical stromal regulators associated with poor prognosis and metastasis in NB remain poorly characterized. This study aimed to identify key cancer-associated fibroblast (CAF)-related genes and to investigate the clinical significance, biological function, and molecular mechanism of FKBP10 in NB malignant progression. Methods: Multi-cohort bioinformatic analyses, including weighted gene co-expression network analysis, machine learning-based LASSO-Cox modeling, and single-cell transcriptomics were performed to screen core stromal biomarkers. In vitro functional assays, rescue experiments, drug sensitivity assays, and in vivo xenograft models were used to validate the oncogenic role of FKBP10 in NB. Results: High CAF infiltration correlated with unfavorable prognosis in NB. FKBP10 was identified as a core stromal effector highly expressed in fibroblasts and malignant NB cells. The FKBP10-based signature effectively stratified patient prognosis in primary and validation cohorts. Mechanistically, FKBP10 facilitated extracellular matrix (ECM) remodeling and mesenchymal reprogramming, accompanied by tumor immune evasion and therapeutic resistance. Functional assays demonstrated that FKBP10 depletion suppressed NB proliferation, migration, invasion, and tumor growth, while restoring FKBP10 rescued malignant phenotypes and reduced chemosensitivity. Conclusions: FKBP10 promotes aggressive NB progression by regulating stromal activation, ECM remodeling and malignant behaviors. FKBP10 serves as a reliable prognostic biomarker and a promising therapeutic target for high-risk neuroblastoma.

Keywords

Neuroblastoma; FKBP10; cancer-associated fibroblasts; tumor microenvironment; extracellular matrix; tumor progression

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