The Cyclin-like Protein Spy1 Regulates Growth and Division Characteristics of the CD133+ Population in Human Glioma

• Spy1 levels are prognostic for poor survival in human glioma
• Spy1 drives proliferation and stemness properties in human glioma
• Spy1 levels are critical for fate of neural cells with stem/progenitor properties
• Spy1 plays an important role in symmetric division of glioma stem cells

SummaryThe heterogeneity of brain cancers, as most solid tumors, complicates diagnosis and treatment. Identifying and targeting populations of cells driving tumorigenesis is a top priority for the cancer biology field. This is not a trivial task; considerable variance exists in the driving mutations, identifying markers, and evolutionary pressures influencing initiating cells in different individual tumors. Despite this, the ability to self-renew and differentiate must be conserved to reseed a heterogeneous tumor mass. Focusing on one example of a tumor-initiating cell population, we demonstrate that the atypical cyclin-like protein Spy1 plays a role in balancing the division properties of glioma cells with stemness properties. This mechanistic insight may provide new opportunities for therapeutic intervention of brain cancer.

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