Stable overexpression of MEN1 suppresses tumorigenicity of RAS

Y. S. Kim, A. L. Burns, P. K. Goldsmith, C. Heppner, S. Y. Park, S. C. Chandrasekharappa, F. S. Collins, A. M. Spiegel, S. J. Marx

Research output: Contribution to journalArticlepeer-review

103 Scopus citations


Although there is indirect genetic evidence that MEN1, the gene for multiple endocrine neoplasia type 1, is a tumor suppressor gene, little is known about the MEN1-encoded protein, menin. Menin was stably overexpressed in a well-characterized murine tumor cell line, (valine-12)-RAS-transformed NIH3T3 cells. Menin overexpression reverted the morphology of the RAS-transformed NIH3T3 cells towards the more flattened and more spread, fibroblastic shape of wild type NIH3T3 cells. The proliferation rate of the RAS-transformed cells in 0.5% calf serum was also slower with menin overexpression. Menin overexpression reduced the RAS-induced clonogenicity in soft agar. Menin also reduced tumor growth after injection of cells in nude mice. In conclusion, stable overexpression of MEN1 suppressed partially the RAS-mediated tumor phenotype in vitro and in vivo. Overexpressed menin protein had biological effects, directly supporting MEN1 gene function as a tumor suppressor.

Original languageEnglish (US)
Pages (from-to)5936-5942
Number of pages7
Issue number43
StatePublished - Oct 21 1999
Externally publishedYes


  • Menin, MEN1
  • NIH3T3
  • Neoplasia
  • Oncogene
  • RAS
  • Tumor suppressor

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research


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