The active vitamin D metabolite 1α,25-dihydroxyvitamin D<sub>3</sub> (1α,25(OH)<sub>2</sub>D<sub>3</sub>) acts as an anti-proliferative agent in human cancer by inhibiting the Wnt/beta-catenin pathway through the vitamin D receptor (VDR).
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 suppression of β‑catenin decreased cancer stem cell (CSC)‑like phenotypes, indicating that β‑catenin is involved in CUG2‑mediated CSC‑like phenotypes.
LF3, a 4-thioureido-benzenesulfonamide derivative and an inhibitor of β-catenin/TCF4 interaction, has been shown to block the self-renewal capacity of cancer stem cells.
In accordance with β-catenin's role in (cancer) stem cell maintenance, the expressions of various stem cell markers, such as <i>AXIN2</i> and <i>LGR5</i>, were reduced and concomitantly differentiation-associated genes were increased.
More importantly, pharmacological activation of Wnt/β-catenin signalling restored the shear stress-suppressed β-catenin expression in LCSCs, and abolished the shear stress-altered sphere-forming ability, chemotherapeutic drug sensitivity, cancer stem cell marker expression, Young's modulus and in vivo tumorigenicity potential of LCSCs.
CTNNB1, encoding β-catenin, is frequently mutated in hepatocellular carcinoma, the most rapidly growing solid cancer in the US, and activating mutations in this gene are associated with increased expression of glutamine synthetase.A new report by Adebayo Michael et al.
In contrast, the Zbed3 mutant failed to enhance β-catenin expression (P > 0.05), and its ability to promote cancer cell proliferation and invasiveness was much less than wild-type Zbed3 (P < 0.05).
Because β-catenin is also essential for normal cells, strategies to specifically target cancer will require identification of druggable factors capable of distinguishing β-catenin signaling pathways between cancer and normal cells.
We also demonstrated, for the first time to the best of our knowledge that exposure to anti-CDH11 antibody suppresses metastasis, reduces CDH11, FN and β-catenin expression, and abrogate the cancer stem cell (CSC)-like traits of MBC cells.
MTDH overexpression in GC cells is associated with EMT and development of cancer stem cell malignant phenotypes and affects the subcellular translocation of β-catenin.
Abnormal expression of O-Linked β-N-acetylglucosamine (O-GlcNAc) and β-catenin is a general feature of cancer and contributes to transformed phenotypes.
We have summarized the impact of HDIs on epithelial (E-cadherin, β-catenin) and mesenchymal (N-cadherin, vimentin) markers, EMT activators (<i>TWIST</i>, <i>SNAIL</i>, <i>SLUG</i>, <i>SMAD</i>, <i>ZEB</i>), as well as morphology, migration and invasion potential of cancer cells.
In primary CRC cells and HCT-8 cells, P2-T3A6 decreased expression of genes regulated by β-catenin and genes associated with cancer stem cells and decreased cell viability and migration.
Here, we provide a review shedding light on the coupling between Wnt/β-catenin activation levels and fluctuations across processes and cellular systems; in particular, we focus on development, in vitro pluripotency maintenance, and cancer.
PRP‑1 significantly decreases the ALDHhigh cancer stem cell population and regulates the aberrant Wnt/β‑catenin pathway in human chondrosarcoma JJ012 cells.
Small ubiquitin related modifier (SUMO)‑specific protease 2 (SENP2) can act as a suppressor in various types of cancer by regulating the stability of β‑catenin to affect the Notch signaling pathway; however, it has a low expression level in CLL cells.
In the mature healthy liver, the Wnt-β-catenin pathway is mostly inactive but can become re-activated during cell renewal and/or regenerative processes, as well as in certain pathological conditions, diseases, pre-malignant conditions and cancer.
Using data from The Cancer Genome Atlas, from the LIRI-JP (Liver Cancer - RIKEN, JP project), and from our transcriptomic, transfection and mouse transgenic experiments, we identify a GRN which functionally links LIN28B-dependent dedifferentiation with dysfunction of β-catenin (CTNNB1).
This study demonstrated that AJAP1 acted as a putative tumor suppressor while β-catenin nuclear localization positively fed back on EGF/EGFR-attenuated AJAP1 expression in breast cancer, which might be beneficial to develop new therapeutic targets for decreasing nuclear β-catenin-mediated malignancy in breast cancer.