NDLI: Celecoxib and radioresistant glioblastoma-derived CD133+ cells: improvement in radiotherapeutic effects. Laboratory investigation.

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Celecoxib and radioresistant glioblastoma-derived CD133+ cells: improvement in radiotherapeutic effects. Laboratory investigation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ma, Hsin-I Chiou, Shih-Hwa Hueng, Dueng-Yuan Tai, Lung-Kuo Huang, Pin-I Kao, Chung-Lan Chen, Yi-Wei Sytwu, Huey-Kang
Description	Country affiliation: Taiwan Author Affiliation: Ma HI ( Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. uf004693@mail2000.com.tw)
Abstract	OBJECT: Glioblastoma, the most common primary brain tumor, has a poor prognosis, even with aggressive resection and chemoradiotherapy. Recent studies indicate that CD133(+) cells play a key role in radioresistance and recurrence of glioblastoma. Cyclooxygenase-2 (COX-2), which converts arachidonic acid to prostaglandins, is over-expressed in a variety of tumors, including CD133(+) glioblastomas. The COX-2-derived prostaglandins promote neovascularization during tumor development, and conventional radiotherapy increases the proportion of CD133(+) cells rather than eradicating them. The aim of the present study was to investigate the role of celecoxib, a selective COX-2 inhibitor, in enhancing the therapeutic effects of radiation on CD133(+) glioblastomas. METHODS: Cells positive for CD133 were isolated from glioblastoma specimens and characterized by flow cytometry, then treated with celecoxib and/or ionizing radiation (IR). Clonogenic assay, cell irradiation, cell cycle analysis, Western blot, and xenotransplantation were used to assess the effects of celecoxib alone, IR alone, and IR with celecoxib on CD133(+) and CD133(-) glioblastoma cells. Three separate xenotransplantation experiments were carried out using 310 severe combined immunodeficient (SCID) mice: 1) an initial tumorigenicity evaluation in which 3 different quantities of untreated CD133(-) cells or untreated or pretreated CD133(+) cells (5 treatment conditions) from 7 different tumors were injected into the striatum of 2 mice (210 mice total); 2) a tumor growth study (50 mice); and 3) a survival study (50 mice). For these last 2 studies the same 5 categories of cells were used as in the tumorigenicity (untreated CD133(-) cells, untreated or pretreated CD133(+) cells, with pretreatment consisting of celecoxib alone, IR alone, or IR and celecoxib), but only 1 cell source (Case 2) and quantity (5 × 10(4) cells) were used. RESULTS: High levels of COX-2 protein were detected in the CD133(+) but not the CD133(-) glioblastoma cells. The authors further demonstrated that 30 µM celecoxib was able to effectively enhance the IR effect in inhibiting colony formation and increasing IR-mediated apoptosis in celecoxib-treated CD133(+) glioblastoma cells. Furthermore, reduction in radioresistance was correlated with the induction of G2/M arrest, which was partially mediated through the increase in the level of phosphorylated-cdc2. In vivo xenotransplant analysis further confirmed that CD133(+)-associated tumorigenicity was significantly suppressed by celecoxib treatment. Importantly, pretreatment of CD133(+) glioblastoma cells with a combination of celecoxib and IR before injection into the striatum of SCID mice resulted in a statistically significant reduction in tumor growth and a statistically significant increase in the mean survival rate of the mice. CONCLUSIONS: Celecoxib combined with radiation plays a critical role in the suppression of growth of CD133(+) glioblastoma stemlike cells. Celecoxib is therefore a radiosensitizing drug for clinical application in glioblastoma.
File Format	HTM / HTML
ISSN	00223085
e-ISSN	19330693
Journal	Journal of Neurosurgery
Issue Number	3
Volume Number	114
Language	English
Publisher	American Association of Neurological Surgeons
Publisher Date	2011-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Neurosurgery Antigens, Cd Metabolism Antineoplastic Agents Pharmacology Brain Neoplasms Drug Therapy Radiotherapy Glioblastoma Glycoproteins Peptides Pyrazoles Sulfonamides Animals Apoptosis Drug Effects Blotting, Western Enzymology Celecoxib Cell Division Cell Line, Tumor Cell Separation Culture Media Cyclooxygenase 2 Biosynthesis Drug Resistance, Neoplasm Flow Cytometry Fluorescent Antibody Technique G2 Phase In Situ Nick-end Labeling Mice Mice, Scid Neoplastic Stem Cells Radiation Effects Survival Analysis Up-regulation Xenograft Model Antitumor Assays Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Neurology (clinical) Surgery

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