In summary, our study demonstrated that TXNDC12 could activate β-catenin via protein-protein interaction and promote ZEB1-mediated EMT and HCC metastasis.
Overall, our results revealed that ETV4 is a novel transcription factor regulated by the S100A8/A9-MCAM axis, which leads to EMT through ZEB1 and thereby to metastasis in breast cancer cells.
While extensive evidence confirmed the importance of ZEB1 as an EMT transcription factor that promotes tumor invasiveness and metastasis, little is known about its regulation.
As expected, AZD5153 treatment significantly reduced the migration of gastric cancer cells overexpressing Mus81 <i>in vitro</i> and <i>in vivo</i> Collectively, we show that Mus81 is a regulator of ZEB1 and promotes metastasis in gastric cancer.
The results showed MAGE-A11 and transcription factors (SP1,TFCP2 and ZEB1) expression were associated with some clinical features in patients, such as pathological differentiation, tumor size, clinical stage, lymph node metastasis and distant metastasis.
By integrating microenvironment signals and being implicated in feedback regulatory loops, ZEB1 appears to be a central switch that determines EMT and metastasis of cancer cells.
Together, this study demonstrates that ATF4-ZEB1 is important for HER2-mediated cell migration and suggests that ATF4-ZEB1 may be potential therapeutic targets for breast cancer metastasis.
Mechanistically, circ-TSPAN4 directly interacted with miR-665, but not miR-4731-5p, to increase the expression of ZEB1, which is a well-known metastasis trigger.
This signal circuit was essential for regulating the expression of epithelial mesenchymal transition (EMT) factors, such as Snail, Zeb1, E-cadherin, and matrix metalloproteinase 9, involved in HCC cell migration and metastasis.
Upregulation of SNHG6 expression induced RKO and HCT116 cell proliferation as well as RKO cell metastasis, while downregulation of SNHG6 expression supressed the proliferation and metastasis of RKO cells and tumor growth <i>in vivo.</i> UPF1 was upregulated and ZEB1 was decreased when SNHG6 knockdown, regulating the TGF-β/Smad pathway and inducing EMT respectively.