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Updated: Mar 22, 2026

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
Published on: November 28, 2015
PRG3 induces Ras-dependent oncogenic cooperation in gliomas.
Zheng Fan1, Philipp Bittermann-Rummel1, Eduard Yakubov1,2
1Translational Neurooncology Laboratory, Department of Neurosurgery, University Hospital Erlangen, Friedrich-Alexander University of Erlangen-Nürnberg (FAU), Erlangen, Germany.
The neuronal gene PRG3 promotes malignant glioma growth by cooperating with Ras signaling. Dysregulated PRG3 levels enhance tumor proliferation and invasion, worsening patient outcomes.
Area of Science:
- Neuro-oncology
- Cancer Genetics
- Molecular Biology
Background:
- Malignant gliomas exhibit cellular heterogeneity and genetic alterations.
- Gene expression disturbances contribute to glioma's aggressive nature.
Purpose of the Study:
- Investigate the role of the neuronal-associated gene PRG3 in glioma.
- Determine PRG3's oncogenic cooperation with Ras signaling pathways.
Main Methods:
- Analysis of PRG3 expression levels in human malignant brain tumors.
- Functional studies involving PRG3 and Ras signaling components.
- In vivo xenograft models to assess glioma progression.
Main Results:
- Perturbed PRG3 levels (elevated or down-regulated) observed in gliomas.
- Imbalanced PRG3 promotes Ras-driven proliferation and migration; angiogenesis is unaffected.
- PRG3 interacts with RasGEF1; C-terminal deletion inhibits Ras.
- PRG3 silencing confers resistance to Ras inhibition.
- In vivo models show PRG3 imbalance exacerbates proliferation, invasion, and clinical outcome.
Conclusions:
- PRG3 acts as an oncogenic partner in gliomas, amplifying malignancy.
- Interference with PRG3 homeostasis significantly impacts glioma progression and patient prognosis.
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