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Updated: Jun 8, 2025

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FKBP4 promotes glycolysis and hepatocellular carcinoma progression via p53/HK2 axis

Zhenzhen Zeng1,2, Shasha Xu1,2, Ruihua Wang3,4

  • 1Department of Nuclear Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Scientific Reports
|November 6, 2024
PubMed

Insights

FKBP4 protein promotes hepatocellular carcinoma (HCC) growth and glycolysis by regulating the p53/HK2 pathway. Targeting FKBP4 offers a potential new therapeutic strategy for HCC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • FKBP4 (FK506-binding protein 4) is implicated in various disorders, but its role in hepatocellular carcinoma (HCC) is unclear.
  • Understanding FKBP4's function in HCC is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate FKBP4 expression, function, and molecular mechanisms in HCC.
  • To explore FKBP4's role in HCC progression and glycolysis.

Main Methods:

  • Bioinformatic analysis of TCGA, ICGC, and GEO datasets.
  • Quantitative RT-PCR and Western blot analyses.
  • Cell proliferation, migration, and glucose uptake assays.
  • FKBP4 and p53 knockdown experiments.

Main Results:

  • FKBP4 is upregulated in HCC tissues and cell lines, correlating with poor prognosis.
  • FKBP4 knockdown inhibits HCC cell proliferation, migration, and glycolysis (glucose/lactic acid/FDG uptake).
  • FKBP4 promotes HCC glycolysis via the p53-mediated HK2 signaling pathway, enhancing p53 stability.

Conclusions:

  • FKBP4 plays a significant role in promoting HCC development and glycolysis.
  • The p53/HK2 signaling pathway is a key mechanism through which FKBP4 influences HCC.
  • Targeting FKBP4 presents a promising therapeutic avenue for HCC treatment.

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