Human Molecular Genetics, 2002, Vol. 11, No. 1 69-76
© 2002 Oxford University Press
Transduction of wild-type merlin into human schwannoma cells decreases schwannoma cell growth and induces apoptosis
Molecular Neurobiology Laboratory, Department of Neurology and 1Department of Pediatric Hematology/Oncology, Heinrich-Heine University Medical Center, Düsseldorf, Germany and 2Zentrum für klinische Forschung, Department of Neurology, University of Ulm, Ulm, Germany
Mutations in both alleles of the tumour suppressor gene coding for merlin/schwannomin, an ERM family protein, cause the hereditary disease neurofibromatosis type 2 (NF2). NF2 is characterized by the development of multiple nervous system tumours especially vestibular schwannomas. Efficient oncoretrovirus-mediated gene transfer of different merlin constructs was used to stably re-express wild-type merlin in primary cells derived from human schwannomas. Using two-parameter FACS analysis we show that expression of wild-type merlin in NF2 cells led to significant reduction of proliferation and G0/G1 arrest in transduced schwannoma cells. In addition, we show increased apoptosis of schwannoma cells transduced with wild-type merlin. Our findings in primary schwannoma cells from NF2 patients strongly support the hypothesis of merlin acting as a tumour suppressor and may help in understanding development of human schwannomas in NF2.
+ To whom correspondence should be addressed. Tel: +49 731 50033645; Fax: +49 731 50033609; Email: oliver.hanemann@medizin.uni-ulm.de
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