Table 1 Various modulators of ZEB1 expression

TGF-β

*

Making complex with SMADs and co-activators and involved in pathways (WNT, RAS, and Notch) to induce EMT

[22, 33, 80,81,82,83,84,85]

miR200c

*

Through ROS/miR-200c/ZEB1 axis suppresses ZEB1 and increase E-Cadherin

[60, 86,87,88]

ERK1/2

*

Directly activated ZEB1 via ERK/ZEB1 signaling pathway

[78, 79]

NF-kB

*

Activation of NF-kB signaling due to different markers such as IL-7 and MUC1 leads to ZEB1 induction

[22, 89]

AKT

*

It has an induction effect on ZEB1 through PI3K/AKT/mTOR

[66, 67, 69, 90, 91]

ASSP2

*

Correlated with the PI3K/AKT pathway

[71]

TKB1

*

Augmenting GSK-3B which is deterrence on radiation-induced EMT by repressing ZEB1

[64]

MiR-200

*

Works as a suppressor of ZEB1 and tumor invasion

[29, 54, 72, 92]

MUC1

*

Creating a complex with ZEB1 intermediating

NF-κB p65 leads to miR-200c repression and contributes to EMT activation

[60]

Snail

*

Corporation with ZEB1 and TGFβ to increase tumor invasiveness

[63]

miR-33b

*

Inactivation of the Wnt/β-catenin/ZEB1 pathway concludes to EMT silencing

[76, 77]

PI3K

*

Involves in different pathways in the induction of EMT

[65,66,67,68, 70, 72, 90]

ESE1

*

Downregulating through the MEK–ERK pathway, resulted in overexpression of ZEB and EMT upregulation

[78]

miR-708

*

Suppressing ZEB1 resulted in EMT reduction

[68]

miR-199a-5p

*

Suppressing ZEB1 resulted in EMT reduction

[69]