e_re22( EMT ):
The gene expressions of MMP-1, MMP-3, and MMP-9 and gelatinolytic activity of MMP-9 were significantly increased in high ETS-1 expression cells.
Low ETS-1 expression cells could not spread on a vitronectin substratum, and the phosphorylation of focal adhesion kinase was markedly impaired because of the reduced expression of integrin b3
TCF8 (ZEB1) regulates cell invasion and migration via MMP1 expression.
TCF8 is likely to be dispensable for endothelial cell motility.
One possible mechanism underlying the increased invasiveness and migration might be the up-regulated digestion of ECMs via TCF8-mediated transcriptional regulation of the gene encoding MMP1.
MMP1 induction during tube formation was significantly enhanced in Matrigel when TCF8 was silenced
MiR-200b Regulates Ets-1-associated Genes
Suppression of endogenous miR-200b induced MMP-1 and VEGFR2 expressions
Overexpression of Ets-1 did not completely reverse miR- 200b-associated MMP-1 and VEGFR2 down-regulation.
It indicates that miR-200b, apart from targeting Ets-1, might silence other target proteins involved in transcription of the indicated genes.
e_re26( EMT ):
TCF3 (E47) is upregulated by Snail1, Snail2, Zeb1.
e_re32( EMT ):
ZEB1 represses PATJ* expression
Knock down of LIN7 results in loss of expression of PATJ*
e_re356( EMT ):
Six1 induces ZEB1 and EMT through transcriptional repression of miR200.
Feedback loop between ZEB1, ZEB2 and MIR200 family
ZEB1 inhibits expression of MIR200 family
SNAI1 represses expression of all MIR200 family members.
e_re366( EMT ):
SNAI1 inhibits miR-203
SNAI1 represses miR-203 and miR-200b expression
p53 activates expression of miR-203
Feedback loop: ZEB1 inhibits expression of MIR203 and MIR183
ZEB1 directly controls transcription of the miR-203 and miR-183 and miR-200 family genes
ZEB2 inhibits expression of MIR203
e_re375( EMT ):
TCF8 (ZEB1) is a negative regulator of angiogenesis in vitro, ex vivo, and in vivo.
e_re1136( EMT ):
e_re1198( EMT ):
Protein expression of Bmi1, Sox2, p63 was reduced after ZEB1 knockdown.
ZEB1 knockdown not only resulted in reduced invasion and metastasis, but also in reduced tumorigenicity.
ZEB1 is also necessary for the self-renewing capacity.
ZEB1 is crucial for drug resistance in pancreatic cancer cells. This supports data showing that EMT activators (Twist and Snail) confer anti-apoptotic properties
e_re1200( EMT ):
Expression of Bmi1, Sox2, p63 was reduced after ZEB1 knockdown.
In compartment: Nucleus
Participates in complexes:
In compartment: Nucleus
Participates in reactions:
As Reactant or Product:
- rZEB1@Nucleus → ZEB1@Nucleus
- ZEB1@Nucleus + LMO2@Nucleus → LMO2:ZEB1@Nucleus
- ZEB1@Nucleus + SMAD2_3*:SMAD4@Nucleus → SMAD2_3*:SMAD4:ZEB1@Nucleus
- ZEB1@Nucleus → Angiogenesis@Nucleus
- gMIR183@Nucleus → arMIR183@Nucleus
- rBMI1@Nucleus → BMI1@Cytoplasm
- rSOX2@Nucleus → SOX2@Nucleus
- gMMP1@Nucleus → rMMP1@Nucleus
- gVEGFA@Nucleus → rVEGFA@Nucleus
- gTCF3@Nucleus → rTCF3@Nucleus
- gE-Cadherin*@Nucleus → rE-Cadherin*@Nucleus
- gPATJ*@Nucleus → rPATJ*@Nucleus
- gMIR200*@Nucleus → arMIR200*@Nucleus
- gMIR203@Nucleus → arMIR203@Nucleus