FKBP9

Last update 08 May 2025

Basic Info

Synonyms

63 kDa FK506-binding protein, 63 kDa FKBP, FK506-binding protein 9

+ [9]

Introduction

PPIases accelerate the folding of proteins during protein synthesis.

100 Clinical Results associated with FKBP9

100 Translational Medicine associated with FKBP9

0 Patents (Medical) associated with FKBP9

Literatures (Medical) associated with FKBP9

01 Mar 2025·Cancer Medicine

Integrated Analysis to Reveal Heterogeneity of Tumor‐Associated Neutrophils in Glioma

Article

Author: Wang, Siyu ; Zheng, Zhiyao ; Wang, Wen ; Zhao, Jizong ; He, Qiheng ; Li, Junsheng ; Sun, Wei ; Mou, Siqi ; Zhang, Bojian ; Liu, Chenglong

ABSTRACTBackgroundGlioma, characterized by its cellular and molecular heterogeneity, presents formidable challenges in treatment strategy and prognostic assessment. The tumor microenvironment (TME) profoundly influences tumor behavior and treatment response, with tumor‐associated neutrophils (TANs) playing a complex but understudied role. This study aimed to investigate the heterogeneity and role of TANs in glioma and to develop a prognostic model.MethodsAnalysis of scRNA‐seq data identified cellular subpopulations and differentially expressed neutrophil‐related genes (DE‐NRGs). Bulk RNA‐seq was obtained from four independent datasets. Molecular subtypes of glioma samples were determined by consensus clustering. WGCNA was conducted to elucidate the association between gene modules and subtypes. We developed a risk score model. Expression of selected genes was confirmed using immunohistochemistry (IHC). In vitro experiments were also performed for functional verification, including CCK8, EdU, Transwell, and TUNEL assays.ResultsA total of 108 DE‐NRGs for TANs were identified based on scRNA‐seq data. Two molecular subtypes were characterized, showing significant differences in prognosis and clinical features. Immune‐related analyses demonstrated varied immunological characteristics between subtypes. The risk score model was constructed with 7 genes, including AEBP1, CAVIN1, DCTD, DEPP1, DUSP6, FKBP9, and UGCG. It showed significant prognostic value and was validated across three external datasets. The mutation landscape highlighted higher IDH mutation prevalence in low‐risk groups. Drug sensitivity analysis indicated TMZ resistance in high‐risk groups. In vitro experiments showed that UGCG could promote glioma cell proliferation, migration, and invasion, while decreasing apoptosis.ConclusionThis study explored the heterogeneity of TANs and developed a prognostic model, providing insights for prognostic prediction and guiding personalized treatment strategies in glioma.Declaration of Generative AI in Scientific Writing: The authors declare nonuse of generative AI and AI‐assisted technologies in the writing process.

01 Nov 2024·Genes & Diseases

The stability of FKBP9 maintained by BiP is crucial for glioma progression

Article

Author: Sun, Bin ; Yang, Hua ; Li, Shirong ; Kong, Qingpeng ; Gao, Jing ; Xia, Wangxiao ; Zhou, Hu ; Yang, Dong ; He, Shuai ; Peng, Weiyan ; Zhu, Yongjie ; Xiang, Tingxiu ; Zhao, Xudong

FK506-binding protein 9 (FKBP9) is involved in tumor malignancy by resistance to endoplasmic reticulum (ER) stress, and the up-regulation of FKBP9 is associated with patients' poor prognosis. The current knowledge of the molecular mechanisms is still limited. One previous study showed that FKBP9 could confer glioblastoma cell resistance to ER stress through ASK1-p38 signaling. However, the upstream regulatory mechanism of FKBP9 expression is still indistinct. In this study, we identified the FKBP9 binding proteins using co-immunoprecipitation followed by mass spectrometry. Results showed that FKBP9 interacted with the binding immunoglobulin protein (BiP). BiP bound directly to FKBP9 with high affinity. BiP prolonged the half-life of the FKBP9 protein and stabilized the FKBP9 protein. BiP and FKBP9 protein levels were positively correlated in patients with glioma, and patients with high expression of BiP and FKBP9 showed a worse prognosis. Further studies showed that FKBP9 knockout in genetically engineered mice inhibited intracranial glioblastoma formation and prolonged survival by decreasing cellular proliferation and ER stress-induced CHOP-related apoptosis. Moreover, normal cells may depend less on FKBP9, as shown by the absence of apoptosis upon FKBP9 knockdown in a non-transformed human cell line and overall normal development in homozygous knockout mice. These findings suggest an important role of BiP-regulated FKBP9-associated signaling in glioma progression and the BiP-FKBP9 axis may be a potential therapeutic target for glioma.

01 Sep 2024·International Immunopharmacology

Machine learning-based autophagy-related prognostic signature for personalized risk stratification and therapeutic approaches in bladder cancer

Article

Author: Wei, Yong ; Lin, Yun-Zhi ; You, Qi ; Cai, Hai ; Xu, Ning ; Lin, Fei ; Huang, Xu-Yun ; Zheng, Qing-Shui ; Wang, Zhen ; Zhu, Jun-Ming ; Xue, Xue-Yi ; Chen, Dong-Ning

OBJECTIVEBladder cancer (BCa) is a highly lethal urological malignancy characterized by its notable histological heterogeneity. Autophagy has swiftly emerged as a diagnostic and prognostic biomarker in diverse cancer types. Nonetheless, the currently accessible autophagy-related signature specific to BCa remains limited.METHODSA refined autophagy-related signature was developed through a 10-fold cross-validation framework, incorporating 101 combinations of machine learning algorithms. The performance of this signature in predicting prognosis and response to immunotherapy was thoroughly evaluated, along with an exploration of potential drug targets and compounds. In vitro and in vivo experiments were conducted to verify the regulatory mechanism of hub gene.RESULTSThe autophagy-related prognostic signature (ARPS) has exhibited superior performance in predicting the prognosis of BCa compared to the majority of clinical features and other developed markers. Higher ARPS is associated with poorer prognosis and reduced sensitivity to immunotherapy. Four potential targets and five therapeutic agents were screened for patients in the high-ARPS group. In vitro and vivo experiments have confirmed that FKBP9 promotes the proliferation, invasion, and metastasis of BCa.CONCLUSIONSOverall, our study developed a valuable tool to optimize risk stratification and decision-making for BCa patients.

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FKBP9

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