The results suggest that E2 upregulates the expression of <i>NFKB1</i>, <i>ATF7IP</i>, and <i>HDAC5</i>, all of which are involved in the regulation of gene expression and transcription, but downregulates that of <i>TCF7L2</i>, <i>ALCAM</i>, and <i>AKT</i>, which are involved in Wnt receptor signaling through β-catenin and morphogenesis in U2OS osteosarcoma cells.
These results demonstrated that artesunate can inhibit β-catenin expression and cell proliferation as well as promote cell apoptosis in MG-63 cells, which indicates that artesunate may serve as a promising drug in the clinical treatment of osteosarcoma.
In conclusion, our results supported a model in which the DNA methylation-mediated down-regulation of miR-370 reduced its inhibitory effect on FOXM1, thereby promoting FOXM1-β-catenin interaction and activating the Wnt/β-Catenin signaling pathway in human osteosarcoma cells.
These findings suggest that miR-135b mediates the constitutive activation of Wnt/β-catenin and Notch signaling, and that the inhibition of miR-135b is a novel strategy to inhibit tumor metastasis and prevent CSC-induced recurrence in OS.
Moreover, the level of β-catenin and its target genes, including c-myc, cyclinD1, and survivin significantly decreased in baicalein-treated osteosarcoma cells, whereas exogenous expression of β-catenin could reverse the anti-proliferative and anti-metastatic effects of baicalein.
We analyzed protein levels and nuclear localization of β-catenin and RUNX2 in a panel of human osteosarcoma cell lines (SAOS, MG63, U2OS, HOS, G292, and 143B).
Up-regulation of β-catenin plays a role in potentiating expression and downstream anti-apoptotic factor Bcl-2, and in enhancing ADM resistance of osteosarcoma U2OS cells.
After SOST gene silencing, the mRNA and protein expression levels of Wnt1, β-catenin, C-Myc, Cyclin D1, and MMP-7 in osteosarcoma cells and β-catenin protein expression levels in the nucleus and cytoplasm were significantly elevated.
In conclusion, our research verified that suppression of CAT104 exerted significant inhibitory effects on osteosarcoma cell proliferation, migration, and invasion by regulating the expression of miR-381 and downstream ZEB1, as well as JNK and Wnt/β-catenin pathways.
In this study, we investigated the vital function of MALAT1 in the progression of OS and its potential leading mechanism, altering the expression and localization of β-catenin via epigenetic transcriptional regulation by interacting with EZH2.
CRY2 knockdown also increased the expression of matrix metalloproteinase (MMP)-2 and β-catenin, and increased OS cell proliferation and migration by inducing cell cycle progression and promoting mitogen-activated protein kinase (MAPK) and Wnt/β-catenin signaling pathways.
Higher expression of miR-940, β-catenin, and cyclinD1 and lower SFRP1 expression were identified in OS tissues. miR-940 targeted and negatively regulated SFRP1 expression.
Finally, we revealed that silybin inhibited OS cell viability by altering the protein levels of β-catenin and Runt-related transcription factor 2 (RUNX2) as determined by western blot and immunocytochemistry (ICC).
We also demonstrated that β-catenin was overexpressed in OS tissue, and that knockdown of β-catenin induced pronounced apoptosis of OS cells in the presence or absence of 17-AAG.