P-REX2a driving tumorigenesis by PTEN inhibition

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Abstract

The phosphatase PTEN (phosphatase and tensin homolog deleted on chromosome 10) antagonizes phosphoinositide 3-kinase (PI3K) signaling and is one of the most frequently mutated tumor suppressors in human cancers. Its regulation appears complex and is of great potential clinical importance. The protein P-REX2a (phosphatidylinositol 3,4,5-trisphosphate Rac exchanger 2a), better known as a regulator of the small guanosine triphosphatase Rac, has been identified as a direct regulator of PTEN activity and as a potential oncoprotein. P-REX2a can stimulate cell proliferation by inhibiting PTEN and stimulating downstream PI3K-dependent signaling. This suggests that aberrant control of PTEN by P-REX2a may represent a key tumorigenic mechanism, in agreement with recent studies supporting the pathological relevance of several other proposed PTEN regulators.
Original languageEnglish
Pages (from-to)pe68
JournalScience Signaling
Volume2
Issue number94
DOIs
Publication statusPublished - 27 Oct 2009

Keywords

  • Cell Transformation, Neoplastic
  • GTPase-Activating Proteins
  • Guanine Nucleotide Exchange Factors
  • Humans
  • PTEN Phosphohydrolase
  • Phosphatidylinositol 3-Kinases
  • Point Mutation
  • Signal Transduction

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