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Beclin 1, an autophagy gene essential for early embryonic development, is a haploinsufficient tumor suppressor.

The biochemical properties of beclin 1 suggest a role in two fundamentally important cell biological pathways: autophagy and apoptosis. We show here that beclin 1-/- mutant mice die early in embryogenesis and beclin 1+/- mutant mice suffer from a high incidence of spontaneous tumors. These tumors continue to express wild-type beclin 1 mRNA and protein, establishing that beclin 1 is a haploinsufficient tumor suppressor gene. Beclin 1-/- embryonic stem cells have a severely altered autophagic response, whereas their apoptotic response to serum withdrawal or UV light is normal. These results demonstrate that beclin 1 is a critical component of mammalian autophagy and establish a role for autophagy in tumor suppression. They both provide a biological explanation for recent evidence implicating beclin 1 in human cancer and suggest that mutations in other genes operating in this pathway may contribute to tumor formation through deregulation of autophagy.

Pubmed ID: 14657337

Authors

  • Yue Z
  • Jin S
  • Yang C
  • Levine AJ
  • Heintz N

Journal

Proceedings of the National Academy of Sciences of the United States of America

Publication Data

December 9, 2003

Associated Grants

None

Mesh Terms

  • Animals
  • Apoptosis
  • Apoptosis Regulatory Proteins
  • Autophagy
  • Embryo, Mammalian
  • Gene Deletion
  • Genes, Tumor Suppressor
  • Membrane Proteins
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Mice, Transgenic
  • Microscopy, Electron
  • Models, Genetic
  • Mutation
  • Neoplasms
  • Proteins
  • RNA, Messenger
  • Time Factors
  • Ultraviolet Rays