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Overexpression of E2F1 in glioma-derived cell lines induces a p53-independent apoptosis that is further enhanced by ionizing radiation

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, CA 94143

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

Abstract

Glioma cell lines show variable responses to radiation in a manner influenced by their p53 status. Irradiation of glioma cell lines does not generally induce apoptosis. When wild-type p53 is present, these cells undergo a G₁ arrest that is closely associated with increased radiosensitivity as measured by clonogenic survival. Previously, others have shown that dysregulated overexpression of E2F1 induces apoptosis in cell lines with either functional or inactivated p53. We found that regardless of p53 status, apoptosis induced by overexpression of E2F1 in glioma cell lines was further enhanced by treatment with ionizing radiation. BAX induction did not follow E2F1 overexpression or irradiation in the glioma cell lines tested. Thus, the apoptotic response of glioma-derived cells to irradiation can be enhanced by E2F1 by a mechanism that does not involve the induction of BAX.

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