TY - JOUR
T1 - Complexity in interpretation of embryonic epithelial-mesenchymal transition in response to transforming growth factor-β signaling
AU - Ahmed, Shaheen
AU - Nawshad, Ali
PY - 2007/6
Y1 - 2007/6
N2 - Epithelial-mesenchymal transition (EMT) is a highly conserved and fundamental process that governs morphogenesis in development and may also contribute to cancer metastasis. Transforming growth factor (TGF-β) is a potent inducer of EMT in various developmental and tumor systems. The analysis of TGF-β signal transduction pathways is now considered a critically important area of biology, since many defects occur in these pathways in embryonic development. The complexity of TGF-β signal transduction networks is overwhelming due to the large numbers of interacting constituents, complicated feedforward, feedback and crosstalk circuitry mechanisms that they involve in addition to the cellular kinetics and enzymatics that contribute to cell signaling. As a result of this complexity, apparently simple but highly important questions remain unanswered, that is, how do epithelial cells respond to such TGF-β signals? System biology and cellular kinetics play a crucial role in cellular function; omissions of such a critical contributor may lead to inaccurate understanding of embryonic EMT. In this review, we identify and explain why certain conditions need to be considered for a true representation of TGF-β signaling in vivo to better understand the controlled, yet delicate mechanism of embryonic EMT.
AB - Epithelial-mesenchymal transition (EMT) is a highly conserved and fundamental process that governs morphogenesis in development and may also contribute to cancer metastasis. Transforming growth factor (TGF-β) is a potent inducer of EMT in various developmental and tumor systems. The analysis of TGF-β signal transduction pathways is now considered a critically important area of biology, since many defects occur in these pathways in embryonic development. The complexity of TGF-β signal transduction networks is overwhelming due to the large numbers of interacting constituents, complicated feedforward, feedback and crosstalk circuitry mechanisms that they involve in addition to the cellular kinetics and enzymatics that contribute to cell signaling. As a result of this complexity, apparently simple but highly important questions remain unanswered, that is, how do epithelial cells respond to such TGF-β signals? System biology and cellular kinetics play a crucial role in cellular function; omissions of such a critical contributor may lead to inaccurate understanding of embryonic EMT. In this review, we identify and explain why certain conditions need to be considered for a true representation of TGF-β signaling in vivo to better understand the controlled, yet delicate mechanism of embryonic EMT.
KW - Epithelial-mesenchymal transitions, embryonic
KW - Transforming growth factor-β
UR - http://www.scopus.com/inward/record.url?scp=34250738303&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34250738303&partnerID=8YFLogxK
U2 - 10.1159/000101314
DO - 10.1159/000101314
M3 - Article
C2 - 17587819
AN - SCOPUS:34250738303
SN - 1422-6405
VL - 185
SP - 131
EP - 145
JO - Cells Tissues Organs
JF - Cells Tissues Organs
IS - 1-3
ER -