P-REX2a driving tumorigenesis by PTEN inhibition

Nick R Leslie

doi:10.1126/scisignal.294pe68

P-REX2a driving tumorigenesis by PTEN inhibition

Nick R Leslie

Research output: Contribution to journal › Article › peer-review

6 Citations (Scopus)

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 language	English
Pages (from-to)	pe68
Journal	Science Signaling
Volume	2
Issue number	94
DOIs	https://doi.org/10.1126/scisignal.294pe68
Publication status	Published - 27 Oct 2009

Keywords

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

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1126/scisignal.294pe68

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title = "P-REX2a driving tumorigenesis by PTEN inhibition",

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.",

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

author = "Leslie, {Nick R}",

year = "2009",

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AU - Leslie, Nick R

PY - 2009/10/27

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N2 - 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.

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.

KW - Cell Transformation, Neoplastic

KW - GTPase-Activating Proteins

KW - Guanine Nucleotide Exchange Factors

KW - Humans

KW - PTEN Phosphohydrolase

KW - Phosphatidylinositol 3-Kinases

KW - Point Mutation

KW - Signal Transduction

U2 - 10.1126/scisignal.294pe68

DO - 10.1126/scisignal.294pe68

M3 - Article

C2 - 19861688

SN - 1945-0877

VL - 2

SP - pe68

JO - Science Signaling

JF - Science Signaling

IS - 94

ER -

P-REX2a driving tumorigenesis by PTEN inhibition

Abstract

Keywords

UN SDGs

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