Related Experiment Video

Updated: May 19, 2026

Quantitative Measurement of Invadopodia-mediated Extracellular Matrix Proteolysis in Single and Multicellular Contexts
14:23

Quantitative Measurement of Invadopodia-mediated Extracellular Matrix Proteolysis in Single and Multicellular Contexts

Published on: August 27, 2012

PCIF1 modulates glioblastoma cell migration and invasion by altering PI(3,4)P2 levels through the PI5-phosphatase

Preethi Priyanka Musunuru1,2, Yihan Li1,2, Yu Zhou1,2

  • 1Department of Neurosurgery, The Affiliated Hospital of Xuzhou Medical University, Xuzhou 221002, China.

Acta Biochimica Et Biophysica Sinica
|May 18, 2026
PubMed

Insights

Phosphorylated CTD Interacting Factor 1 (PCIF1) suppresses glioma cell migration and invasion by regulating the AKT pathway and epithelial-to-mesenchymal transition. PCIF1 acts as a tumor suppressor, offering potential therapeutic targets for glioblastoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Phosphorylated CTD Interacting Factor 1 (PCIF1) is crucial for mRNA m6Am modification.
  • Previous studies established PCIF1 as a glioma tumor suppressor, inhibiting proliferation and inducing apoptosis.
  • The role of PCIF1 in glioma cell migration and invasion was previously unclear.

Purpose of the Study:

  • To investigate the role of PCIF1 in regulating glioma cell migration and invasion.
  • To elucidate the molecular mechanisms underlying PCIF1's effects on glioma invasion.
  • To explore PCIF1's potential as a therapeutic target in glioblastoma.

Main Methods:

  • Overexpression and knockdown of PCIF1 in glioma cells.
  • Assessment of cell migration and invasion assays.
  • Analysis of epithelial-to-mesenchymal transition (EMT) markers (Vimentin, β-catenin, Snail, Slug, T-cadherin).
  • Investigation of the AKT signaling pathway and phosphoinositide metabolism (PI(3,4)P2, PI(3,4,5)P3).

Main Results:

  • PCIF1 overexpression inhibited glioma cell migration and invasion.
  • PCIF1 knockdown enhanced migration and invasion, correlating with EMT marker changes.
  • PCIF1 modulated AKT pathway activity through complex regulation of AKT and p-AKT levels.
  • PCIF1 influenced phosphoinositide signaling, affecting AKT activation via INPP5B.

Conclusions:

  • PCIF1 suppresses EMT-mediated glioma invasion.
  • PCIF1 regulates glioblastoma cell migration and invasion via phosphoinositide signaling and AKT pathway modulation.
  • PCIF1 is a potential biomarker and therapeutic target for glioma.

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