The majority of @entity5 develop genetic and molecular strategies to resist conventional cytotoxic therapies as well as escape from the host's immune surveillance. These events lead to @entity5 persistence and spread through activation of the epithelial to mesenchymal transition (EMT) program and @entity3 . Expression profiling analysis has revealed @entity5 @entity3 -inducing and @entity3 -suppressing genes that regulate the metastatic process and maintain the microenvironment of the @entity5 cells. EMT in @entity5 entails the molecular reprogramming and phenotypic changes that characterize the conversion of immobile @entity5 epithelial cells to motile mesenchymal cells. A hallmark of EMT is the loss of @entity5962 , the epithelial homotypic adhesion molecule, and gain of mesenchymal markers such as @entity2277 and fibronectin. The molecular mechanisms underlying the initiation of EMT consist, in part, in the constitutive activation of survival signaling pathways such as the nuclear factor (NF)-kB pathway. The NF-kB pathway has been implicated directly in the regulation of EMT and indirectly through the transcription and expression of several gene products that participate in the EMT cascade, such as @entity4245 , the @entity3 -inducer and @entity5962 suppressor transcription factor. In turn, @entity4245 represses the @entity3 -suppressor gene product @entity3218 ( @entity3218 ) that inhibits both the @entity10242 / @entity8047 / @entity3963 and NF-kB survival pathways implicated in EMT. Consequently, @entity5 cells normally exhibit a dysregulated NF-kB/ @entity4245 / @entity3218 circuitry that is intimately involved in the initiation of EMT and maintenance of drug resistance. Additional deregulated gene products in this circuit, such as the @entity3 -suppressor phosphatase and tensin homologue ( @entity983 ; repressed by @entity4245 ) and the putative- @entity3 inducer @entity19767 (target of NF-kB) also have been associated in the regulation of EMT. We recently have investigated the direct role of @entity19767 in the regulation of EMT. This review discusses the molecular regulation of EMT in @entity5 cells through the activity of the dysregulated NF-kB/ @entity4245 / @entity19767 / @entity983 / @entity3218 circuitry. In addition, we propose @entity19767 as a potential novel prognostic biomarker for EMT and a therapeutic target for both the prevention of @entity3 and the reversal of resistance.

The novel role of @entity19767 in the regulation of epithelial to mesenchymal transition in XXXX via the dysregulated NF-kB/ @entity4245 / @entity19767 / @entity3218 / @entity983 Circuitry.

@entity8047 :: ('5609', 'Gene') :: ['MEK'] @entity4245 :: ('6615', 'Gene') :: ['Snail'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor', 'various tumor', 'cancers', 'cancer'] @entity3218 :: ('5037', 'Gene') :: ['RKIP', 'Raf-kinase inhibitor protein'] @entity5962 :: ('999', 'Gene') :: ['E-cadherin'] @entity3963 :: ('5594', 'Gene') :: ['ERK'] @entity983 :: ('5728', 'Gene') :: ['PTEN'] @entity2277 :: ('7431', 'Gene') :: ['vimentin'] @entity3 :: ('MESH:D009362', 'Disease') :: ['metastasis'] @entity10242 :: ('5894', 'Gene') :: ['Raf-1'] @entity19767 :: ('7528', 'Gene') :: ['Yin Yang (YY) 1', 'YY1']
@entity5 :: (MESH:D009369,Disease) :: ['cancer']
