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Neuro-Oncology 2001 3(2):113-122; doi:10.1093/neuonc/3.2.113
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© 2001 by the Society forNeuro-Oncology

Introduction of mutant p53 into a wild-typep53-expressing glioma cell line confers sensitivity to Ad-p53-inducedapoptosis

Julie A. Cerrato, W.K. Alfred Yung and Ta-Jen Liu2

Department of Neuro-Oncology, The University of Texas M.D. AndersonCancer Center, Houston, Texas 77030

2 Address correspondence and reprint requests to Ta-Jen Liu, Box 100, Departmentof Neuro-Oncology, The University of Texas M.D. Anderson Cancer Center, 1515Holcombe Blvd., Houston, TX 77030.


  Abstract

Transient expression of the tumor suppressor gene p53 viaadenoviral-mediated gene transfer induces apoptosis in glioma cells expressingmutant p53, while causing cell cycle arrest in cells with wild-typep53. To determine whether a change in p53 status of awild-type p53-expressing cell line such as U-87 MG would alter itsapoptotic resistant phenotype in response to Ad-p53 infection, wegenerated cell lines U-87-175.4 and U-87-175.13 via retroviral-mediated genetransfer of the p53 (175H) mutant into the U-87 MG parental line.Control cell lines U-87-Lux.6 and U-87-Lux.8 were also generated and expressthe reporter gene luciferase. Both U-87-175.4 and U-87-175.13, but not controlcell lines, exhibited morphology characteristic of apoptosis after Ad-p53infection. Furthermore, expression of other p53 mutants (248W, 273H)in U-87 MG also sensitized cells to Adp53-induced apoptosis. Apoptosis wasconfirmed by TUNEL and cell cycle analysis. Several p53 responsegenes were examined in cells infected with Ad-p53, and among these, BCL2,p21WAF1/CIP1, CPP32/caspase 3, and PARP showeddifferences in expression between U87-175 and U87-Lux cell lines. Takentogether, our data demonstrate that the introduction of p53 mutantsin U-87 MG promotes an apoptotic response in association withadenoviral-mediated wild-type p53 gene transfer. These resultsunderscore the importance of glioma p53 genotype for predicting tumorresponse to p53-based gene therapy.

Received July 17, 2000; Accepted November 2, 2000


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