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Updated: Jan 7, 2026

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections
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Choline kinase α interacts with epidermal growth factor receptor to activate the mitogen-activated protein kinase

Yourui Zou1, Xiao Wu2, Yang Liu1

  • 1Department of Neurosurgery, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, China.

Chinese Medical Journal
|December 31, 2025
PubMed
Abstract

Insights

Choline kinase alpha (CHKA) drives glioma malignancy by regulating epidermal growth factor receptor (EGFR) and activating the MAPK pathway. Targeting the CHKA/EGFR/MAPK axis offers a promising therapeutic strategy for glioma.

Area of Science:

  • Neuro-oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Glioma is an aggressive brain tumor with limited treatment options.
  • The precise regulatory mechanisms of Choline kinase α (CHKA) in glioma progression are not fully understood.

Purpose of the Study:

  • To investigate the role of CHKA in glioma progression.
  • To elucidate the relationship between CHKA, epidermal growth factor receptor (EGFR), and the mitogen-activated protein kinase (MAPK) pathway in glioma.
  • To evaluate the CHKA/EGFR axis as a potential therapeutic target.

Main Methods:

  • Single-cell RNA sequencing to assess CHKA and EGFR coexpression in glioma.
  • Analysis of public datasets and clinical cohorts for relevance.
  • Immunohistochemistry for expression and localization.
  • Mass spectrometry, coimmunoprecipitation, PCR, and Western blotting to examine interactions and pathway activation.
  • In vitro assays (CCK-8, transwell, wound-healing) and in vivo xenograft models to assess functional impact.

Main Results:

  • CHKA is highly coexpressed with EGFR in specific glioma subpopulations and correlates with advanced grade and poor prognosis.
  • CHKA interacts with and promotes EGFR expression and phosphorylation, subsequently activating the MAPK pathway.
  • CHKA knockdown inhibits glioma cell proliferation, migration, and invasion, while EGFR overexpression rescues these effects.
  • In vivo, CHKA inhibition suppresses tumor growth and MAPK activation, with EGFR restoration reversing these outcomes.

Conclusions:

  • CHKA promotes glioma malignancy by regulating EGFR and activating the MAPK pathway.
  • The CHKA/EGFR/MAPK signaling axis is a critical driver of glioma progression.
  • This axis presents a potential therapeutic target for glioma treatment.
Keywords:
Choline kinase αEGFRGliomaMAPK pathwayMigrationSingle-cell RNA-sequencingXenograft model

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