ArticleExperimental and therapeutic medicine2020
FKBP51 induces p53-dependent apoptosis and enhances drug sensitivity of human non-small-cell lung cancer cells.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Sexually distinct multi-omic responses to progressive endurance exercise training in the rat lung.American journal of respiratory cell and molecular biology · 2026Article
- Novel Candidate Genes Involved in an Initial Stage of White Striping Development in Broiler Chickens.Animals : an open access journal from MDPI · 2024Article
- An Overview of the Deubiquitinase USP53: A Promising Diagnostic Marker and Therapeutic Target.Current protein & peptide science · 2024Review
- FKBP51 promotes invasion and migration by increasing the autophagic degradation of TIMP3 in clear cell renal cell carcinoma.Cell death & disease · 2021Article
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Authors and funding
23 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is one of the most prevalent cancer types worldwide, and non-small-cell lung cancer (NSCLC) accounts for ~85% of all lung cancer cases. Despite the notable prevalence of NSCLC, the mechanisms underlying its progression remain unclear. The present study investigated the involvement of FK506-binding protein 51 (FKBP51) in NSCLC development and determined the factors associated with FKBP51 modification for NSCLC treatment. Immunohistochemical analysis was performed to analyze FKBP51 expression in human NSCLC tissue samples. Additionally, flow cytometry was performed to observe the apoptosis of FKBP51-overexpressing A549 cells. A dual-luciferase reporter assay was performed to confirm the association between FKBP51 and p53 expression, and western blotting was performed to analyze the effects of FKBP51 on the p53 signaling pathway. Finally, cell viability was measured using a Cell Counting Kit-8 assay. The results suggested FKBP51 downregulation in human lung cancer. Furthermore, apoptosis rates may be increased in FKBP51-overexpressing A549 cells. Moreover, FKBP51 promoted p53 expression and subsequent p53 signaling pathway activation. These results indicated that FKBP51 promoted A549 cell apoptosis via the p53 signaling pathway. Additionally, FKBP51 enhanced the sensitivity of A549 cells to cisplatin. Collectively, these data suggested that FKBP51 could serve as a biomarker for human lung cancer and can thus be tailored for incorporation into NSCLC therapy in the future.
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