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P4HA2 Promotes Epithelial-to-Mesenchymal Transition and Glioma Malignancy through the Collagen-Dependent PI3K/AKT

Jing Lin1,2, Lei Jiang3, Xiaogang Wang4

  • 1Department of Neurosurgery, The 452 Hospital of Western Air Force, Chengdu 600021, China.

Journal of Oncology
|August 26, 2021
PubMed

Insights

Prolyl-4-hydroxylase subunit 2 (P4HA2) drives glioma progression by promoting cell proliferation, migration, and invasion. Inhibiting P4HA2 or its collagen modification activity suppresses glioblastoma growth and impacts PI3K/AKT signaling.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Prolyl-4-hydroxylase subunit 2 (P4HA2) is implicated in extracellular matrix remodeling and cancer.
  • The specific role of P4HA2 in glioma, particularly glioblastoma, is not well understood.

Purpose of the Study:

  • To investigate the expression, oncogenic functions, and molecular mechanisms of P4HA2 in glioblastoma.
  • To determine the relationship between P4HA2 and patient survival in glioma.

Main Methods:

  • Analysis of TCGA datasets and patient paraffin samples for P4HA2 expression.
  • Utilizing lentivirus for P4HA2 knockdown and an AKT agonist (SC79) to study its functions.
  • Employing a P4HA2 inhibitor (DHB) to explore underlying molecular pathways.

Main Results:

  • P4HA2 is overexpressed in glioma, correlating inversely with patient survival.
  • P4HA2 knockdown inhibited glioma cell proliferation, migration, invasion, and EMT in vitro, and suppressed tumor growth in vivo.
  • P4HA2 inhibition downregulated collagen gene expression and phosphorylated PI3K/AKT signaling, effects reversed by AKT activation.

Conclusions:

  • P4HA2 acts as an oncogenic molecule in glioblastoma.
  • P4HA2 promotes glioma malignancy by regulating collagen expression and the PI3K/AKT pathway.
  • Targeting P4HA2 may represent a therapeutic strategy for glioblastoma.

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