Treatment of β-catenin siRNA-transfected cells with a specific inhibitor of nuclear factor-kappaB (NF-κB), SN50, significantly reduced enhancement of uPA, uPAR and PAI-1 expression and cancer cell invasion, observed in β-catenin siRNA-transfected cells.
The common role of beta-catenin in both Wnt signaling and cell adhesion provides a unique opportunity to develop chemopreventive therapies that both prevent the development of cancer and delay tumor progression.
We showed further that up-regulated TrpC5 caused a robust rise in intracellular calcium concentration [Ca<sup>2+</sup>]<sub>i</sub>, increased Wnt5a expression and the nuclear translocation of β-catenin, leading to a reduction in cancer differentiation and an increase in cancer cell stemness.
Glioma is one of the most treatment-refractory intracranial tumors, and the aberrant expressed Wnt/β-catenin pathway is closely associated with glioma malignancy.
The oncogenic beta-catenin/T-cell factor (TCF) signal is a common trigger inducing expressions of various cancer-related genes and is activated in various types of human malignancy.
From this analysis we identified: (i) the nodes linking the three molecular networks specific for kidney, bladder and prostate cancer; (ii) the relative HUB nodes (RXRA, MAP3K7, NR3C1, PABPC1, NDRG1, RELA and CTNNB1) that link the three cancer networks; (iii) the miRNAs able to target these HUB nodes.
Furthermore, the expression of B-cell lymphoma 2 (Bcl-2), the pro-form of caspase-7 (pro-caspase-7), β-catenin and c-Myc was downregulated, while that of ephrin receptor (EphA5), a biomarker of cancer cell dormancy, was slightly increased in these two tumor cell lines treated with hUCMSC-CM.
We found the expression of beta-catenis is higher in cancer tissues than in normal kidney tissues and the level of beta-catenin is associated with the tumor stage.
MicroRNA-21 promotes tumour malignancy via increased nuclear translocation of β-catenin and predicts poor outcome in APC-mutated but not in APC-wild-type colorectal cancer.
These findings suggest that CD44 and beta-catenin expression may have an important role in the development of malignancy and in the determination of biological features of keratoacanthoma and squamous cell carcinoma of the skin.
Overexpression of IL-35 in colon cancer cell suppressed cell migration, invasion, proliferation, colony formation and cancer stem cells through suppressing β-catenin.
A thorough understanding of interactions between β-catenin and its binding partners will enable us to more effectively understand how β-catenin switches between its multiple roles, and will lead to the development of specific assays for the identification of small molecules as chemotherapeutic agents to treat diseases, including cancer and neurological disorders, where Wnt/β-catenin signaling is dysregulated.
Although it has been reported that abnormal activation of the Wnt/beta-catenin-dependent pathway is often observed in human prostate cancer, the involvement of the beta-catenin-independent pathway in this cancer is unclear.
Because beta-catenin and its target genes urokinase-type plasminogen activator receptor (uPAR) and cyclin D1 are overexpressed in colon cancers, and are linked to cancer growth, invasion, and metastasis, we investigated whether DCA activates beta-catenin signaling and promotes colon cancer cell growth and invasiveness.
Together, this may suggest that two molecular pathways, intermediate methylation associated with KRAS mutations and LST-G morphology, and low methylation associated with CTNNB1 activation and LST-NG morphology, might be involved in LST development, and that involvement of TP53 mutations could be important in both subtypes in the development from adenoma to cancer.
Overexpression of IL-37 in colon cancer cell suppressed cell migration, invasion, proliferation, colony formation and cancer stem cells through suppressing β-catenin.
High levels of beta-catenin and activating mutations in the beta-catenin gene (CTNNB1) have been demonstrated in malignant melanomas, implicating dysregulated Wnt signalling in the pathogenesis of this malignancy.