ArticleScientific reports2024
FKBP4 promotes glycolysis and hepatocellular carcinoma progression via p53/HK2 axis.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- USP7-dependent stabilization of FKBP4 contributes to acquired osimertinib resistance through glycolytic remodeling in NSCLC.Scientific reports · 2026Article
- The regulatory role of circGDI2 in hepatocellular carcinoma proliferation and glycolysis with the involvement of m6A modification.Non-coding RNA research · 2026Article
- IGF2BP1 orchestrates glycolytic reprogramming via HK2 to accelerate hepatocellular carcinoma malignancy.American journal of cancer research · 2026Article
- Machine learning integration of bulk and single-cell RNA-seq data reveals glycolytic heterogeneity in colorectal cancer.Medical oncology (Northwood, London, England) · 2025Article
- FKBP prolyl isomerase 4: a potential target for heart failure and cardioprotective effects via leonurine-pretreated mesenchymal stem cell-derived exosomes.Stem cell research & therapy · 2025Article
- Increased expression of chaperone proteins in response to DENV 2 infection of Huh-7 liver cells.PloS one · 2025Article
- Assessment of prognosis and responsiveness to immunotherapy in colorectal cancer patients based on the level of immune cell infiltration.Frontiers in immunology · 2025Article
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Authors and funding
4 authors.
Funding
Abstract
FKBP4, a member of the FK506-binding protein (FKBP) family, is a promising target for a variety of disorders, including cancer. However, its underlying molecular mechanism and potential function in hepatocellular carcinoma (HCC) are largely elusive. Therefore, we aimed to investigate the expression status, functional implications and underlying mechanisms of FKBP4 in HCC. Our bioinformatics analysis of TCGA LIHC datasets, ICGC LIRI-JP datasets and GEO datasets results showed FKBP4 was upregulated in HCC tissues. We also confirmed the elevated FKBP4 in clinical HCC samples. Additionally, quantitative RT-PCR results revealed FKBP4 was highly expressed in all five tested HCC cell lines. We also observed a correlation between elevated FKBP4 expression and poor prognosis in HCC patients. Loss of FKBP4 can inhibit the proliferation and migration in HCC cells. Furthermore, we found that silencing FKBP4 suppressed glucose uptake, lactic acid production and
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