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Updated: Jul 30, 2025

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
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AKR1B1 Represses Glioma Cell Proliferation through p38 MAPK-Mediated Bcl-2/BAX/Caspase-3 Apoptotic Signaling Pathways

Yu-Kai Huang1,2,3, Kun-Che Chang1,4,5, Chia-Yang Li1

  • 1Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.

Current Issues in Molecular Biology
|May 15, 2023
PubMed

Insights

Aldo-keto reductase family 1 member B1 (AKR1B1) inhibits glioma cell proliferation by activating p38 MAPK signaling, influencing apoptosis. AKR1B1 may be a novel therapeutic target for glioma treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Glioma, a prevalent brain tumor, exhibits complex regulatory mechanisms influencing cell proliferation and apoptosis.
  • Aldo-keto reductase family 1 member B1 (AKR1B1) is implicated in various cellular processes, but its specific role in glioma remains to be fully elucidated.
  • Understanding the molecular pathways governing glioma progression is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To investigate the regulatory role of AKR1B1 in glioma cell proliferation.
  • To determine the involvement of p38 MAPK activation in AKR1B1-mediated apoptosis signaling.
  • To explore the potential of AKR1B1 as a therapeutic target for glioma.

Main Methods:

  • Quantitative real-time PCR to assess AKR1B1 expression in glioma tissues and cell lines.
  • MTT assay and Western blot to evaluate the effects of AKR1B1 modulation and p38 MAPK inhibition on cell proliferation and apoptosis-related proteins (Bcl-2, BAX, caspase-3).
  • Annexin V-FITC/PI staining to confirm AKR1B1-induced apoptosis.

Main Results:

  • AKR1B1 expression was significantly downregulated in glioma tissues and glioblastoma cell lines.
  • AKR1B1 overexpression inhibited glioma cell proliferation, while knockdown increased it.
  • AKR1B1 induced p38 MAPK phosphorylation, leading to increased BAX and caspase-3 activity and decreased Bcl-2 expression, ultimately promoting apoptosis.

Conclusions:

  • AKR1B1 plays a critical role in regulating glioma cell proliferation and apoptosis.
  • The p38 MAPK signaling pathway is a key mediator of AKR1B1's effects on apoptosis.
  • AKR1B1 represents a promising therapeutic target for the development of novel glioma treatments.
Keywords:
AKR1B1BAXBcl-2caspase-3glioblastomap38 MAPK

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