ArticleArchives of medical science : AMS2015
FK506-binding protein 5 inhibits proliferation and stimulates apoptosis of glioma cells.
Article in Archives of medical science : AMS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Deepening the Understanding of Platelet-Derived RNA as Biomarker for Glioblastoma Through GSEA, TDEA, and Elastic Net Regularization Analysis.Cancer reports (Hoboken, N.J.) · 2026Article
- Role of FK506 binding protein 51 in central nervous system diseases.Frontiers in molecular neuroscience · 2025Review
- FKBP5 associated CD8 T cell infiltration is a novel prognostic biomarker in luminal B breast cancer.The Journal of international medical research · 2023Article
- Peripheral mRNA Expression and Prognostic Significance of Emotional Stress Biomarkers in Metastatic Breast Cancer Patients.International journal of molecular sciences · 2022Article
- FKBP51 promotes invasion and migration by increasing the autophagic degradation of TIMP3 in clear cell renal cell carcinoma.Cell death & disease · 2021Article
- FK506-binding protein 5 promotes the progression of papillary thyroid carcinoma.The Journal of international medical research · 2021Article
- Up-regulation of autophagy and apoptosis of cochlear hair cells in mouse models for deafness.Archives of medical science : AMS · 2021Article
- Aberrant expression of long non-coding RNAs (lncRNAs) is involved in brain glioma development.Archives of medical science : AMS · 2020Article
- The function and clinical relevance of lncRNA UBE2CP3-001 in human gliomas.Archives of medical science : AMS · 2018Article
- Comparative analysis of FKBP family protein: evaluation, structure, and function in mammals and Drosophila melanogaster.BMC developmental biology · 2018Review
- USP49 negatively regulates tumorigenesis and chemoresistance through FKBP51-AKT signaling.The EMBO journal · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionFK506-binding protein 5 (FKBP5) is reported to act as a scaffolding protein for Akt to promote the dephosphorylation of AKT Ser473 and suppress pancreatic cancer growth. However, other studies have shown that FKBP5 promotes tumor growth and chemoresistance through regulating NF-κB signaling in other cancers. In this study, we attempted to investigate the role and mechanism of action of FKBP5 in the regulation of proliferation and apoptosis of glioma cells. MATERIAL AND
methodsThe glioma U251 cell line was used as the model. Cell proliferation was detected by MTT assay. Cell apoptosis was detected by annexin-V staining. Protein expression was detected by Western blot analysis.
resultsFKBP5 overexpression inhibited the proliferation of U251 cells significantly (p < 0.05), and promoted the apoptosis of U251 cells significantly (p < 0.05). In addition, FKBP5 overexpression inhibited the phosphorylation of Akt at Ser743, decreased the level of Bcl-2, increased the level of Bax, and enhanced the cleavage of caspase-9 and caspase-3 (p < 0.05 compared to control). In contrast, FKBP5 knockdown enhanced the proliferation of U251 cells, increased the phosphorylation of Akt significantly (p < 0.05), increased the expression of Bcl-2 and decreased the expression of Bax, and decreased the cleavage of caspase-9 and caspase-3 significantly (p < 0.05).
conclusionsFKBP5 plays the role of a tumor suppressor in glioma by inhibiting the activation of Akt and stimulating the intrinsic mitochondrial apoptotic pathway, and could be used as a new target for gene therapy of glioma.
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