RT Journal Article
SR Electronic
T1 P-REX2a Driving Tumorigenesis by PTEN Inhibition
JF Science Signaling
JO Sci. Signal.
FD American Association for the Advancement of Science
SP pe68
OP pe68
DO 10.1126/scisignal.294pe68
VO 2
IS 94
A1 Leslie, Nick R.
YR 2009
UL http://stke.sciencemag.org/content/2/94/pe68.abstract
AB 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.