Fig. 3

Regulation of intracellular and extracellular markers towards EMT. EMT is regulated by intracellular and extracellular markers. Wnt signaling inhibits GSK-3β which is an inhibitor of β-catenin, β-catenin in turn downregulates epithelial marker E-cadherin through influencing transcriptional factors. YAP/TAZ translocates to the nucleus and binds to TEAD to enhance the mesenchymal markers i.e. vimentin and N-cadherin and downregulate E-cadherin. TGF-β signaling can trigger the MAPK/ERK pathway and Smad pathway. Smad inhibits GSK-3β and can activate transcription factors including SNAIL, ZEB, and TWIST, resulting in a loss of cell–cell adhesion and an increase in mesenchymal markers. ERK pathway also contributes to Smad4 at the nucleus in the enhancement of the mesenchymal transcription factors.‘↑’ indicates upregulation, ‘↓’ indicates downregulation. Arrows indicate downstream cellular events/activation and lines indicate inhibition. Akt, Ak strain transforming; EMT, epithelial-mesenchymal transition; GSK-3β, glycogen synthase kinase-3 beta; PTPRB, receptor protein tyrosine phosphatase; TAZ, transcriptional coactivator with PDZ-binding motif; TEAD, transcriptional enhanced associate domain; Wnt, Wingless-related integration site; YAP, yes-associated protein; ZEB, Zinc-finger E-box-binding homeobox