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Neuro-Oncology 2000 2(1):16-21; doi:10.1093/neuonc/2.1.16
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© 2000 by the Society forNeuro-Oncology

Overexpression of E2F1 in glioma-derived cell lines induces ap53-independent apoptosis that is further enhanced by ionizing radiation

Hui-Kuo G. Shu, Carol M. Julin, Felix Furman, Garret L. Yount, Daphne Haas-Kogan and Mark A. Israel2

Preuss Laboratory for Molecular Neuro-oncology,Department of Neurological Surgery (H.-K.G.S., C.M.J., F.F., G.L.Y., D.H.-K.,M.A.I.) and Department of Radiation Oncology(H.-K.G.S., G.L.Y., D.H.-K.), University of California, San Francisco, CA94143

2 Address correspondence and reprint requests to Mark A. Israel, M.D., UCSFBrain Tumor Research Center, Dept. of Neurological Surgery, HSE 722, 505Parnassus, San Francisco, CA 94143-0520.


  Abstract

Glioma cell lines show variable responses to radiation in a mannerinfluenced by their p53 status. Irradiation of glioma cell lines does notgenerally induce apoptosis. When wild-type p53 is present, these cells undergoa G1 arrest that is closely associated with increasedradiosensitivity as measured by clonogenic survival. Previously, others haveshown that dysregulated overexpression of E2F1 induces apoptosis in cell lineswith either functional or inactivated p53. We found that regardless of p53status, apoptosis induced by overexpression of E2F1 in glioma cell lines wasfurther enhanced by treatment with ionizing radiation. BAX inductiondid not follow E2F1 overexpression or irradiation in the glioma cell linestested. Thus, the apoptotic response of glioma-derived cells to irradiationcan be enhanced by E2F1 by a mechanism that does not involve the induction ofBAX.

Received July 20, 1999; Accepted September 23, 1999


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