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Mitogens and the Cell Cycle

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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...

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Updated: Jul 30, 2025

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

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Mitogen-induced defective mitosis transforms neural progenitor cells.

Hiba K Omairi¹, Cameron J Grisdale², Mathieu Meode¹

¹Arnie Charbonneau Cancer Institute, University of Calgary, Calgary, Alberta, Canada.

|May 15, 2023

Summary

Platelet-derived growth factor-A (PDGFA) causes defective mitosis in neural progenitor cells (NPCs), leading to genomic instability and glioblastoma (GBM) development, particularly in P53-deficient cells.

Keywords:

GBM P53 PDGFA kinetochore mitosis

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Systemic Injection of Neural Stem/Progenitor Cells in Mice with Chronic EAE

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Published on: April 15, 2014

Area of Science:

Neuroscience
Cancer Biology
Genetics

Background:

Chromosome instability (CIN) is common in glioblastoma (GBM) but underlying causes are unclear.
Genes regulating cell division are rarely mutated in cancers.
Platelet-derived growth factor-A (PDGFA), a brain mitogen, was investigated for its role in GBM initiation.

Purpose of the Study:

To investigate the effects of PDGFA on neural progenitor cells (NPCs) as a model for GBM initiation.
To understand how PDGFA influences mitosis, gene expression, and genomic stability in NPCs.

Main Methods:

Utilized an in vitro model of high-grade glioma initiation from murine NPCs.
Exposed NPCs to PDGFA and analyzed nuclear/mitotic phenotypes, gene, and protein expression.
Assessed P53-dependent effects on mitosis and cell survival.

Main Results:

PDGFA induced abnormal mitosis in NPCs, with P53-dependent outcomes.
Defective mitosis led to cell death in wild-type cells but was tolerated in P53-null cells.
Surviving P53-null cells accumulated chromosomal rearrangements, forming tumorigenic NPCs with GBM-like genomic alterations.

Conclusions:

PDGFA can transform NPCs by causing defective mitosis and genomic instability, particularly in the absence of P53.
The genomic architecture of GBM may be an adaptation to ensure survival despite mitotic errors.
This study reveals a mechanism for NPC transformation by a brain-associated mitogen, offering insights into GBM pathogenesis.