2. Academic Validation
  3. Anti-cancer effect of targeting fibroblast activation protein alpha in glioblastoma through remodeling macrophage phenotype and suppressing tumor progression

Anti-cancer effect of targeting fibroblast activation protein alpha in glioblastoma through remodeling macrophage phenotype and suppressing tumor progression

  • CNS Neurosci Ther. 2022 Nov 15. doi: 10.1111/cns.14024.
Yazhou Miao 1 2,  Yuxuan Deng 1 2,  Jinqiu Liu 3,  Jing Wang 3,  Boyi Hu 3,  Shuyu Hao 1 2,  Herui Wang 4,  Zhe Zhang 1 2,  Zeping Jin 1 2,  Yang Zhang 1 2,  Chunzhao Li 1 2,  Peng Zhang 1 2,  Hong Wan 3,  Shaodong Zhang 3,  Jie Feng 3 5,  Nan Ji 1 2 6
Affiliations

Affiliations

  • 1 Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
  • 2 National Clinical Research Center for Neurological Diseases (China), Beijing, China.
  • 3 Beijing Neurosurgical Institute, Capital Medical University, Fengtai, Beijing, China.
  • 4 Neuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
  • 5 Beijing Cancer Institute, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, China.
  • 6 Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, School of Engineering Medicine, Beihang University, Beijing, China.
PMID: 36382346 DOI: 10.1111/cns.14024
Abstract

Introduction: Glioblastoma (GBM) is the most malignant form of glioma and has a poor median survival time. Fibroblast activation protein alpha (FAP) is a dual-specificity serine Protease that is strongly associated with the development and progression of human carcinomas. However, relatively little is known about the function of FAP and its potential as a therapeutic target in GBMs.

Aims: In this study, we aimed to explore the role of FAP in GBM through a series of experiments and to evaluate the therapeutic effect of PT100, a small molecule inhibitor of FAP, on GBM.

Results: Increased FAP expression was associated with poor survival in glioma. In vitro, FAP knockdown inhibited the process of EMT and caused a decrease in the number of M2 macrophages. In vivo, PT100 was confirmed to suppress the progression of GBMs significantly.

Conclusions: FAP could serve as a biomarker and novel therapeutic target for the treatment of GBM and that PT100 is a promising drug for the treatment of GBM.

Keywords

PT100; epithelial-mesenchymal transition; fibroblast activation protein alpha; glioblastoma.

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