TY - JOUR
T1 - Epithelial-mesenchymal transition in development and cancer
T2 - Role of phosphatidylinositol 3′ kinase/AKT pathways
AU - Larue, Lionel
AU - Bellacosa, Alfonso
PY - 2005/11/14
Y1 - 2005/11/14
N2 - Epithelial-mesenchymal transition (EMT) is an important process during development by which epithelial cells acquire mesenchymal, fibroblast-like properties and show reduced intercellular adhesion and increased motility. Accumulating evidence points to a critical role of EMT-like events during tumor progression and malignant transformation, endowing the incipient cancer cell with invasive and metastatic properties. Several oncogenic pathways (peptide growth factors, Src, Ras, Ets, integrin, Wnt/β-catenin and Notch) induce EMT and a critical molecular event is the downregulation of the cell adhesion molecule E-cadherin. Recently, activation of the phosphatidylinositol 3′ kinase (PI3K)/AKT axis is emerging as a central feature of EMT. In this review, we discuss the role of PI3K/AKT pathways in EMT during development and cancer with a focus on E-cadherin regulation. Interactions between PI3K/AKT and other EMT-inducing pathways are presented, along with a discussion of the therapeutic implications of modulating EMT in order to achieve cancer control.
AB - Epithelial-mesenchymal transition (EMT) is an important process during development by which epithelial cells acquire mesenchymal, fibroblast-like properties and show reduced intercellular adhesion and increased motility. Accumulating evidence points to a critical role of EMT-like events during tumor progression and malignant transformation, endowing the incipient cancer cell with invasive and metastatic properties. Several oncogenic pathways (peptide growth factors, Src, Ras, Ets, integrin, Wnt/β-catenin and Notch) induce EMT and a critical molecular event is the downregulation of the cell adhesion molecule E-cadherin. Recently, activation of the phosphatidylinositol 3′ kinase (PI3K)/AKT axis is emerging as a central feature of EMT. In this review, we discuss the role of PI3K/AKT pathways in EMT during development and cancer with a focus on E-cadherin regulation. Interactions between PI3K/AKT and other EMT-inducing pathways are presented, along with a discussion of the therapeutic implications of modulating EMT in order to achieve cancer control.
KW - Cadherins/physiology
KW - Cell Transformation, Neoplastic
KW - Epithelial Cells/physiology
KW - Mesoderm/physiology
KW - Neoplasm Invasiveness
KW - Neoplasm Metastasis
KW - Phosphatidylinositol 3-Kinases/metabolism
KW - Proto-Oncogene Proteins c-akt/metabolism
KW - Signal Transduction
UR - http://www.scopus.com/inward/record.url?scp=27844461512&partnerID=8YFLogxK
UR - https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=purepublist2023&SrcAuth=WosAPI&KeyUT=WOS:000233201900007&DestLinkType=FullRecord&DestApp=WOS
U2 - 10.1038/sj.onc.1209091
DO - 10.1038/sj.onc.1209091
M3 - Review article
C2 - 16288291
SN - 0950-9232
VL - 24
SP - 7443
EP - 7454
JO - Oncogene
JF - Oncogene
IS - 50
ER -
