The aberrant nucleocytoplasmic shuttling of active PTK6/β-catenin is reversed by expressing the PSPC1 C-terminal interacting domain (PSPC1-CT131), thereby suppressing PSPC1/PTK6/β-catenin-activated metastasis to prolong the survival of HCC orthotopic mice.
Our findings identify a critical role of FMOD in cancer metastasis, reveal a mechanism regulating FMOD transcription and impacting tumor metastasis, uncover action targets and mechanism for the anticancer activity of Aspirin, and expand the understanding of the Wnt/β-catenin pathway and tumor metastasis, which are valuable for development of cancer therapeutics.
Target sequencing analysis revealed, both in primary tumor and metastasis, a pathogenic KRAS gene missense mutation c.38G > A p.(Gly13Asp) and a likely pathogenic CTNNB1 gene missense mutation c.94G > A p.(Asp32Asn).
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.
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.
In our previous study, succinate dehydrogenase 5 (<i>SDH5</i>) was reported to regulate ZEB1 expression, induce EMT and lead to lung cancer metastasis via the GSK3β/β-catenin pathway.
For the first time, we have observed that LOX-1 inhibition significantly prevents metastasis formation in injected mice and, at the same time, induces a downregulation of VEGF-A165, HIF-1α, and β-catenin whose expression is involved in cell migration and metastasis, and a variation of histone H4 acetylation pattern suggesting also a role of LOX-1 in regulating gene transcription.
In summary, our study demonstrated that TXNDC12 could activate β-catenin via protein-protein interaction and promote ZEB1-mediated EMT and HCC metastasis.
To finally explore the relationship of ACLY and CTNNB1, we used western blots, migration and invasion assays to confirm that ACLY may regulate metastasis by CTNNB1.
The current study demonstrated that treatment with gefitinib decreased the protein expression levels of phosphorylated-GSK3β and β-catenin, which suggests that gefitinib may be a potential novel therapeutic strategy in CC by suppressing the Wnt/β-catenin signaling pathway and EMT to inhibit tumor metastasis in CC cells.
APC2, as one of the target genes, was significantly up-regulated by AQB and led to degradation of β-catenin resulting in suppression of Wnt/β-catenin signaling which may contribute to inhibition of tumor growth and metastasis <i>in vitro</i> and in orthotopic breast cancer models.
Furthermore, the activity of key molecules of the adenomatous polyposis coli (APC)/β‑catenin complex was altered following treatment with BITC, which suggested a potential role for the APC/β‑catenin complex in the BITC‑mediated induction of apoptosis and inhibition of metastasis in murine mammary carcinoma.
Clinicopathologic analysis revealed that increased FOXM1 (or β-catenin) expression positively correlated with some clinicopathologic features, such as tumor size, TNM stage, lymphatic metastasis, and distant metastasis (<i>P</i><0.05).
Except one case of salivary gland AdCC that showed loss of β-catenin expression and developed subsequent metastasis, all AdCCs showed strong and diffuse membranous β-catenin expression.
Enhanced expression of circular RNA hsa_circ_000984 promotes cells proliferation and metastasis in non-small cell lung cancer by modulating Wnt/β-catenin pathway.