Twist  induces epithelial-mesenchymal transition in cervical carcinogenesis by regulating the XXXX / @entity7379 signaling pathway.

@entity1 @entity7379 @entity5 @entity2533 @entity3
UNASSIGNED: Epithelial-mesenchymal transition (EMT) is associated with the @entity3 and poor prognosis of @entity5 . However, the underlying mechanisms are poorly defined. In the present study, we investigated whether Twist  plays a direct role in @entity1 @entity5 using immunohistochemical and western blot analyses. Immunohistochemical analysis revealed that Twist  is highly expressed in @entity5 , which correlates with poor @entity5 pathological differentiation or lymph node @entity3 (P<0.05). Depletion of Twist  by stable shRNA-mediated knockdown decreased the migratory ability of @entity5 cell lines in  vitro. Suppression or overexpression of Twist  also resulted in an altered expression of the molecular mediators of EMT. Furthermore, exogenous @entity2533 promoted EMT by upregulating the expression of Twist  through the @entity2533 / @entity7379 pathway, and this effect was eliminated by Twist  depletion in @entity5 cells as demonstrated in the in  vitro study. The use of in  vivo models revealed a decreased @entity5 proliferation potential in Twist-depleted @entity5 cells. The results suggested a novel function for Twist  in the promotion of EMT via @entity2533 / @entity7379 signaling pathway. Thus, Twist  constitutes a potential therapeutic target in @entity1 @entity5 .
