We identified increased β-catenin and Atk expression was associated with drug resistance and poor prognosis in breast cancer patients using public databases.
Immunohistochemistry (IHC) was performed to assess the prevalence of MAGE-A, vimentin, E-cadherin and β-catenin in breast cancer tissues and correlate them with clinical pathological parameters.
In addition, the Wnt/β-Catenin pathway inhibitor was found to be able to reverse the impact of DCLK1 overexpression on BCa cell proliferative and metastatic capacity.
Furthermore, high levels of stromal TILs as well as CD8+ or FOXP3+ TIL subsets were associated with β-catenin overexpression by breast cancer, respectively.
The abnormal rate of β-catenin expression and the overexpression of cyclin D1 and c-myc were higher in breast carcinomas compared with breast cystic hyperplasia tissues.
We found that the Frizzled 1 (FZD1) protein, which is an essential component of the Wnt/β-catenin pathway, is overexpressed in the multidrug resistant breast cancer cell subline MCF-7/ADM, coincident with MDR1/P-gp.
Although mutation of APC or CTNNB1 (beta-catenin) is rare in breast cancer, activation of Wnt signalling is nonetheless thought to play an important role in breast tumorigenesis, and epigenetic silencing of Wnt antagonist genes, including the secreted frizzled-related protein (SFRP) and Dickkopf (DKK) families, has been observed in various tumours.
Taken together, our results suggested that Mn12Ac inhibited the migration, invasion, and epithelial-mesenchymal transition by regulating Wnt/β-catenin and PI3K/AKT signaling pathways in breast cancer.
Our findings suggest that, in contrast to E-cadherin, mutations of alpha- and beta-catenin do not contribute to the pathogenesis or the diffuse growth patterns of gastric or breast carcinomas.
Overexpression of DVL3 resulted in upregulation of β‑catenin and amplification of breast cancer cell growth, which confirmed that Wnt/β‑catenin activation via DVL3 is associated with breast cancer oncogenesis.
Natural phytochemicals modulate oxidative stress, leptin, integrin, HER2, MAPK, ERK, Wnt/β-catenin and NFκB signaling along with regulating ERα and ERβ, thereby presenting unique opportunities for both primary and combinatorial interventions in BC.
The results indicate that CUL1 knockdown prohibited the metastasis behaviors of breast cancer cells through downregulation (dephosphorylation) of the EMT signaling pathways of EGFR and Akt/GSK3β/β-catenin in breast cancer.
Aryl hydrocarbon receptor/cytochrome P450 1A1 pathway mediates breast cancer stem cells expansion through PTEN inhibition and β-Catenin and Akt activation.
Up-regulation of WNT2 mRNA by estrogen might play a key role in some cases of human breast cancer through activation of the beta-catenin - TCF signaling pathway.
To conclude, our results support the concept that STAT3 upregulates the protein expression and transcriptional activity of β-catenin in breast cancer, and these two proteins may cooperate with each other in exerting their oncogenic effects in these tumors.
These findings provide a new perspective to counteract the invasive behavior of breast cancer, indicating that blocking PI3K-AKT pathway-dependent β-catenin accumulation may represent a potential therapeutic approach to control breast cancer.