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.
Furthermore, lumichrome potentially suppressed cancer stem cells (CSCs) in lung cancer by dramatically suppressing CSC markers together with the CSC-maintaining cell signaling namely protein kinase B (AKT) and β-catenin.
In addition, oncogenes CTNNB1 and FN1 were highly edited and significantly overexpressed in malignantly transformed cell lines, thus may be responsible for the lung cancer progression.
The results indicated that miR-146-5p promoted cell viability, migration and invasion, inhibited apoptosis and activated Wnt/β-catenin and PI3K/AKT/MAPK signal pathways by regulating claudin-12 expression in lung cancer cells.
These results suggest that TRIB3 interacts with β-catenin and thus activates β-catenin signaling, which is responsible for lung cancer progression, and blocking TRIB3 activity might be developed to treat lung cancer.
The effect of si-CCAT2 on the expression of nuclear and cytoplasmic β-catenin protein in the lung cancer NCI-H1975 cell line was detected using western blot analysis.
Associations between environmental variants together with single nucleotide polymorphisms (SNPs) of beta-catenin (ctnnb1) and lung cancer risk were analyzed using a logistic regression model.
Finally, western blot assays demonstrated that there was no difference in β‑catenin and glycogen synthase kinase 3β (GSK‑3β) expression in cancer cells compared with NL‑20, but increased phosphorylated (p‑)β‑catenin and p‑GSK‑3β was detected in lung cancer cell lines compared with NL‑20, particularly in A549 cells.
These results show that PDE10 is overexpressed during lung cancer development and essential for lung tumor cell growth in which inhibitors can selectively induce apoptosis by increasing intracellular cGMP levels and activating PKG to suppress oncogenic β-catenin and MAPK signaling.
Immunohistochemistry assay of tissue microarrays from patients with lung cancer indicated that both CBP and β-catenin were highly expressed in tumor tissues and predicted poor prognosis in lung adenocarcinoma patients.
Mechanistically, we affirmed that QKI-5 reduced β-catenin level in LC cells via suppressing its translation and promoting its degradation, whereas QKI-5 promoter hypermethylation suppressed QKI-5 expression.