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.
RhCG knockdown significantly decreased pH<sub>i</sub> and impeded tumor cellular proliferation, migration and invasion and repressed β-catenin and c-myc expression in GC cells.
In the case of CNF1, it occurs by up-regulation of the transcription factors ZEB1 and Snail1, delocalisation of E-cadherin and β-catenin, activation of the serine/threonine kinase mTOR, accelerated wound healing, and invasion.
Mechanistically, DEPTOR depletion not only activated both mTORC1 and mTORC2 signals to promote cell proliferation and survival, but also induced an AKT-dependent epithelial-mesenchymal transition (EMT) and β-catenin nuclear translocation to promote cell migration and invasion.
These compound mice displayed accelerated prostate tumor formation and invasion compared with their littermates that expressed only stabilized β-catenin.
These findings reveal a novel and instrumental role of KAT2A-mediated histone succinylation in regulation of gene expression and β-catenin stability to promote tumor cell proliferation and invasion.
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.
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.
In conclusion, our data suggest that leptin promotes an increase in the expression levels of Twist and β-catenin, the secretion of MMP-2, MMP-9, the invadopodia formation and invasion in MCF10A cells in a Src and FAK-dependent manner.
lncRNA PLAC2 activated by H3K27 acetylation promotes cell proliferation and invasion via the activation of Wnt/β‑catenin pathway in oral squamous cell carcinoma.
In addition, knockdown of miR-410 promoted the expression of DKK, inhibited CRC cell proliferation, migration and invasion capacity, and induced cell apoptosis, while overexpression of miR-410 reversed these results. miR-410 silencing also decreased β-catenin and pGSK-3β levels.
Furthermore, we demonstrated that adiponentin-AdipoR1 axis inhibits tumor cells migration and invasion by blocking the GSK3β/β-Catenin pathway and enhances sunitinib sensitivity via abrogating PI3K/AKT/NF-κB signaling.
Calcium imaging was applied to detect intracellular Ca<sup>2+</sup> and revealed that <i>H. pylori</i> induced an increase of intracellular Ca<sup>2+</sup> in GC cells through release from Ca<sup>2+</sup> stores and extracellular Ca<sup>2+</sup> influx.Further study indicated that <i>H. pylori</i> infection led to an upregulation of the expression of transient receptor potential cation channel subfamily C member 6 (TRPC6) and induced an increase of Ca<sup>2+</sup> through the TRPC6 channel.Furthermore, <i>H. pylori</i> increased TRPC6 transcription through the Wnt/β-catenin pathway, and Wnt/β-catenin/TRPC6 signaling was identified to be at least in part responsible for <i>H. pylori</i>-induced GC migration and invasion.
The present study elucidates the potential role of Trop2 in tumor invasion and the promotion of epithelial-mesenchymal transition (EMT) when binding β-catenin in GC.
Up-regulated EFEMP2 expression significantly hampered the invasion and metastasis abilities of breast cancer cells and the process of epithelial interstitial transformation (EMT) via the Wnt/β-catenin pathway.
The anti-UNC119 treatment inhibited tumor cell proliferation, growth, migration and invasion by inhibiting the Wnt/β-catenin and GF-β/ EMT signaling pathways, respectively.
Moreover, SERPINB2 overexpression could inhibit the invasion and migration capabilities of CNE2R and CNE2 cells, with downregulation of vimentin, N-cadherin, nuclear β-catenin, matrix metalloproteinase (MMP)-2 and MMP-9, and upregulation of E-cadherin.
The expression of β-catenin in placenta accreta might play an important role in the regulation of placental cell invasion; low expression of β-catenin in placenta accreta might be responsible for excessive trophoblastic invasion.
Suppression of Syncytin 1 inhibited the migration and invasion, as well as the expressions of epithelial-mesenchymal transition (EMT) makers, N-cadherin, β-catenin, and Vimentin, indicating that Syncytin 1 knockdown inhibited the metastasis via reversing the EMT process in A549 cells.
Based on our data, β-catenin may be involved in cancer invasion in pancreatic cancer, and it is not associated with CD44, the invasion related protein.