Next, we developed a quantitative intravital microscopy (qIVM) approach, using a syngeneic lymphatic reporter mouse tumor model, to investigate the effect of systemic ezrin inhibition on cancer cell migration and metastasis.
Recent studies show that ezrin phosphorylation regulates breast cancer metastasis by promoting cancer cell survivor and promotes intrahepatic metastasis via cell migration.
These results suggest that LOXL2-induced ezrin phosphorylation, which also requires PKCα, is critical for LOXL2-induced cytoskeletal reorganization that subsequently promotes tumor cell invasion and metastasis in ESCC.
The expression of Ezrin and matrix metalloprotease-9 (MMP-9), which are two mediator proteins that serve roles in tumor cell migration and invasion, were analyzed in each cell group via western blotting.
Pooled analyses showed that ezrin overexpression was correlated with a higher rate of tumor metastasis (OR 6.59, 95% CI: 2.84-15.33, P < 0.01, P<sub>FDR</sub> < 0.01) and recurrence (OR 3.18, 95% CI: 1.88-5.37, P < 0.01, P<sub>FDR</sub> < 0.01) and a more advanced tumor grade (OR 3.252, 95% CI: 1.371-7.715, P = 0.01, P<sub>FDR</sub> = 0.03).
We conclude that Ezrin is a key downstream factor involved in the regulation of HGF/Met signaling-induced metastasis and demonstrate a link between Ezrin and HGF/Met/MAPK/Sp1 activation in the metastatic process.
The distinguished strong Western blot staining of ezrin E3 in sentinel lymph node metastases underlines its capability to substantiate the occurrence of lymph node (micro)metastases in breast cancer patients.
Hence, we speculated that mutations in the tumor suppressor gene, BRCA1, which is already reported to induce metastasis via abnormal expression of Ezrin, Radixin and Moesin (ERM), could generate MAF.
These findings indicate that ezrin and HER2 expression in patients with SGCs represents a high-grade histopathological subtype that requires adjuvant therapy, including molecularly targeted therapies, to decrease the risk of subsequent metastasis.
Previously, the C-C-motif chemokine ligand 25 (CCL25) was identified to be involved in metastasis and drug resistance in the MOLT4 T-ALL cell line, as was the ezrin protein.
This study reports expression of Ezrin in high lymphatic metastasis (Hca-F >70%) and low metastatic metastasis (Hca-P <30%) HCC cell lines, and the effect of A7 on Ezrin expression.
Finally, knockout of Ezrin inhibited EGF-induced lung metastasis of colorectal cancer xenografts and abnormal activation of Ezrin and NF-kB were related with colorectal cancer metastasis and poor prognosis.