CD44v6 Regulates Growth of Brain Tumor Stem Cells Partially through the AKT-Mediated Pathway
2011

CD44v6 Regulates Growth of Brain Tumor Stem Cells

Sample size: 64 publication 10 minutes Evidence: moderate

Author Information

Author(s): Jijiwa Mayumi, Demir Habibe, Gupta Snehalata, Leung Crystal, Joshi Kaushal, Orozco Nicholas, Huang Tiffany, Yildiz Vedat O., Shibahara Ichiyo, de Jesus Jason A., Yong William H., Mischel Paul S., Fernandez Soledad, Kornblum Harley I., Nakano Ichiro

Primary Institution: The Ohio State University and University of California Los Angeles

Hypothesis

The study investigates the role of CD44v6 in the growth of brain tumor stem cells (BTSC) in glioblastoma multiforme (GBM).

Conclusion

CD44v6 is crucial for the growth of a subset of BTSC in GBM, and targeting this pathway may improve treatment outcomes.

Supporting Evidence

  • Patients with CD44high GBM exhibited significantly poorer prognoses.
  • CD44v6 was the only isoform detected in BTSC.
  • Knockdown of CD44v6 inhibited in vitro growth of BTSC from CD44high GBM.
  • Stimulation with osteopontin increased phosphorylated AKT expression in CD44high GBM.
  • CD44v6 was abundantly expressed by tumor precursors in a mouse model.

Takeaway

This study found that a specific protein called CD44v6 helps some brain cancer cells grow, and blocking it could help treat the cancer better.

Methodology

The study used human tissue samples, animal models, and various assays including RT-PCR, flow cytometry, and neurosphere formation assays to analyze the role of CD44v6.

Potential Biases

Potential biases may arise from the selection of samples and the methods used for analysis.

Limitations

The study's conclusions are based on a limited number of samples and further research is needed to confirm the findings.

Participant Demographics

Patients included in the study were diagnosed with various grades of gliomas, including low grade astrocytoma and GBM.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0024217

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