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Elevated Invasive Potential of Glioblastoma Stem Cells

Overview
Publisher Elsevier
Specialty Biochemistry
Date 2011 Mar 5
PMID 21371437
Citations 118
Authors
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Abstract

Glioblastomas (GBMs) are the most lethal and common types of primary brain tumors. The hallmark of GBMs is their highly infiltrative nature. The cellular and molecular mechanisms underlying the aggressive cancer invasion in GBMs are poorly understood. GBM displays remarkable cellular heterogeneity and hierarchy containing self-renewing glioblastoma stem cells (GSCs). Whether GSCs are more invasive than non-stem tumor cells and contribute to the invasive phenotype in GBMs has not been determined. Here we provide experimental evidence supporting that GSCs derived from GBM surgical specimens or xenografts display greater invasive potential in vitro and in vivo than matched non-stem tumor cells. Furthermore, we identified several invasion-associated proteins that were differentially expressed in GSCs relative to non-stem tumor cells. One of such proteins is L1CAM, a cell surface molecule shown to be critical to maintain GSC tumorigenic potential in our previous study. Immunohistochemical staining showed that L1CAM is highly expressed in a population of cancer cells in the invasive fronts of primary GBMs. Collectively, these data demonstrate the invasive nature of GSCs, suggesting that disrupting GSCs through a specific target such as L1CAM may reduce GBM cancer invasion and tumor recurrence.

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References
1.
Cheng L, Wu Q, Huang Z, Guryanova O, Huang Q, Shou W . L1CAM regulates DNA damage checkpoint response of glioblastoma stem cells through NBS1. EMBO J. 2011; 30(5):800-13. PMC: 3049209. DOI: 10.1038/emboj.2011.10. View

2.
Li Z, Bao S, Wu Q, Wang H, Eyler C, Sathornsumetee S . Hypoxia-inducible factors regulate tumorigenic capacity of glioma stem cells. Cancer Cell. 2009; 15(6):501-13. PMC: 2693960. DOI: 10.1016/j.ccr.2009.03.018. View

3.
Xia H, Qi Y, Ng S, Chen X, Li D, Chen S . microRNA-146b inhibits glioma cell migration and invasion by targeting MMPs. Brain Res. 2009; 1269:158-65. DOI: 10.1016/j.brainres.2009.02.037. View

4.
Bao S, Wu Q, Li Z, Sathornsumetee S, Wang H, McLendon R . Targeting cancer stem cells through L1CAM suppresses glioma growth. Cancer Res. 2008; 68(15):6043-8. PMC: 2739001. DOI: 10.1158/0008-5472.CAN-08-1079. View

5.
Park D, Sathornsumetee S, Rich J . Medical oncology: treatment and management of malignant gliomas. Nat Rev Clin Oncol. 2010; 7(2):75-7. DOI: 10.1038/nrclinonc.2009.221. View