Furthermore, we found that HOXB5 binds directly to the CTNNB1 promoter region and activates the transcriptional expression of β-catenin, as well as its downstream target genes, encoding cyclin D1 and c-Myc, leading to an increase in the invasion and migration activity of human gastric cancer cells.
Furthermore, several functional experiments, including a colony formation assay, CCK-8 assay, wound healing assay and Transwell invasion assay, revealed that miR-885-5p suppressed cell proliferation, migration and invasion through inhibition of β-catenin.
The aberrant expression of E-cadherin and S100A4 not β-catenin in the invasive margin was a significant and independent risk factor for disease-free and overall-survival by multivariate analysis, along with AJCC stage and perineural invasion. mRNA levels of β-catenin and S100A4 were correlated with the IHC findings at the tumor invasive margin.
Furthermore, elevated miR-488 in isolated mouse endometrial glandular endometrial cells inhibited FZD7, the translocation of β-catenin to nucleus, the activation of Wnt pathway, and the cell proliferation, migration and invasion.
Protein kinase D2 contributes to TNF-α-induced epithelial mesenchymal transition and invasion via the PI3K/GSK-3β/β-catenin pathway in hepatocellular carcinoma.
Subsequently, we found that both CXCR4 and β‑catenin antagonists could significantly inhibit the proliferation, colony formation, migration and invasion of SW780 cells.
Wnt7a depletion in 5637 HMI and T24 cells reduced UBC cell invasion and decreased levels of active β-catenin and its downstream target genes involved in the epithelial-to-mesenchymal transition (EMT) and extracellular matrix (ECM) degradation.
Moreover, cell migration and invasion were reduced by over twofold in linc-ITGB1 knockdown cells probably due to upregulation of β-catenin and downregulation of vimentin, slug, and TCF8.
Together, our results indicated that IL-8 triggered ovarian cancer cells migration partly through Wnt/β-catenin pathway mediated EMT, and IL-8 may be an important molecule in the invasion and metastasis of ovarian cancer.
In addition, L1, L5, and VLDL, but not HDL, increased the levels of mesenchymal markers Slug, Vimentin, and β-Catenin, and promoted breast cancer cell migration and invasion.
Aberrant activation of the canonical Wnt/beta-catenin pathway occurs in almost all colorectal cancers and contributes to their growth, invasion and survival.
Thus, by far the most common mutations in colorectal tumors, found in the Wnt-signaling pathway and leading to the stabilizing of beta-catenin, might influence invasion by altering adhesive properties and EMT of tumor cells.
Moreover, the Sirt1 up-regulation resulted in increases in HCC cell proliferation and invasion together with decreases apoptosis, and increases in the cytosolic accumulation and nuclear translocation of the transcription factor β-catenin in vitro.
Approximately 15% of high-intermediate risk patients had unfavorable features (substantial lymphovascular space invasion, p53-mutant, and/or >10% L1CAM), 50% favorable features (POLE-mutant, NSMP being microsatellite stable, and CTNNB1 wild-type), and 35% intermediate features (MSI or CTNNB1-mutant).
The present results indicate that mdig can inhibit the phosphorylation of GSK-3β and promote the phosphorylation and destabilization of β-catenin, in order to suppress the expression of slug, snail, and ZEB1 and the occurrence of EMT, and thereby inhibit the invasion and metastasis of non-small cell lung cancer (NSCLC).
Knock-out of chondroitin 4-<i>O</i>-sulfotransferase-1 (C4ST-1), a key CS biosynthetic enzyme, suppressed activation of the N-cadherin/β-catenin pathway through N-cadherin endocytosis and significantly decreased BT-549 cell invasion.
Three-dimensional organotypic co-culture assays revealed that WNT2-mediated fibroblast motility and extracellular matrix remodeling enhanced cancer cell invasion of cell lines even harboring mutations in the adenomatous polyposis coli/β-catenin pathway.
Collectively, these results suggest that the expression level of migfilin in ESCCs is inversely correlated with clinical metastasis status, and migfilin inhibits ESCC cell invasion at least in part through promoting degradation of β-catenin.