Transduction of wild-type merlin into human schwannoma cells decreases schwannoma cell growth and induces apoptosis

K. M.M. Schulze, C. O. Hanemann, H. W. Müller, H. Hanenberg

Research output: Contribution to journalArticle

62 Scopus citations

Abstract

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-parameters 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.

Original languageEnglish (US)
Pages (from-to)69-76
Number of pages8
JournalHuman molecular genetics
Volume11
Issue number1
DOIs
StatePublished - Jan 1 2002

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Genetics(clinical)

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