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Updated: May 29, 2025

Translational Orthotopic Models of Glioblastoma Multiforme
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PRPF4 Knockdown Suppresses Glioblastoma Progression via the p38 MAPK and ERK Signaling Pathways

Wansoo Kim1,2, Song Park3,4,5, Se-Hyeon Han6

  • 1School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Republic of Korea.

Anticancer Research
|January 31, 2025
PubMed
Abstract

Insights

Pre-mRNA processing factor 4 (PRPF4) knockdown inhibits glioblastoma (GBM) progression by suppressing key signaling pathways and altering cell metabolism. Targeting PRPF4 presents a potential new therapeutic strategy for GBM treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Pre-mRNA processing factor 4 (PRPF4) is a core component of U4/U6 snRNPs, essential for pre-mRNA splicing.
  • PRPF4 also plays roles in cell survival, apoptosis, and oncogenesis, with mutations linked to retinitis pigmentosa.
  • The specific role of PRPF4 in glioblastoma (GBM) progression was previously unclear.

Purpose of the Study:

  • To investigate the functional role of PRPF4 in GBM progression.
  • To evaluate PRPF4 as a potential therapeutic target for GBM.

Main Methods:

  • Gene expression profiling to compare PRPF4 levels in GBM versus normal tissues.
  • Establishment of stable PRPF4 knockdown GBM cell lines (A172, T98G).
  • Assessment of cell proliferation, apoptosis, migration, and invasion; analysis of affected signaling pathways (p38 MAPK, ERK) and metabolic processes via proteomic analysis.

Main Results:

  • PRPF4 expression is elevated in GBM tumors.
  • PRPF4 knockdown significantly reduced GBM cell proliferation, induced apoptosis, and suppressed migration and invasion.
  • Knockdown of PRPF4 affected the MKK3/6-p38-ATF2 and RAS-MEK-ERK1/2 signaling pathways and disrupted metabolic pathways, including glutathione and carbon metabolism.

Conclusions:

  • PRPF4 knockdown inhibits GBM progression by modulating p38 MAPK and ERK signaling pathways and inducing metabolic alterations.
  • Targeting PRPF4 offers a promising novel therapeutic strategy for GBM treatment.
Keywords:
EMTERK signalingGlioblastomaPRPF4apoptosisp38 MAPK signalingproliferation

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