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2016 ; 5
(2
): ä Nephropedia Template TP
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Role of EMT in Metastasis and Therapy Resistance
#MMPMID26828526
Smith BN
; Bhowmick NA
J Clin Med
2016[Jan]; 5
(2
): ä PMID26828526
show ga
Epithelial-mesenchymal transition (EMT) is a complex molecular program that
regulates changes in cell morphology and function during embryogenesis and tissue
development. EMT also contributes to tumor progression and metastasis. Cells
undergoing EMT expand out of and degrade the surrounding microenvironment to
subsequently migrate from the primary site. The mesenchymal phenotype observed in
fibroblasts is specifically important based on the expression of smooth muscle
actin (?-SMA), fibroblast growth factor (FGF), fibroblast-specific protein-1
(FSP1), and collagen to enhance EMT. Although EMT is not completely dependent on
EMT regulators such as Snail, Twist, and Zeb-1/-2, analysis of upstream signaling
(i.e., TGF-?, EGF, Wnt) is necessary to understand tumor EMT more
comprehensively. Tumor epithelial-fibroblast interactions that regulate tumor
progression have been identified during prostate cancer. The cellular crosstalk
is significant because these events influence therapy response and patient
outcome. This review addresses how canonical EMT signals originating from
prostate cancer fibroblasts contribute to tumor metastasis and recurrence after
therapy.
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