RFC3 induces epithelial‑mesenchymal transition in lung adenocarcinoma cells through the Wnt/β‑catenin pathway and possesses prognostic value in lung adenocarcinoma.
Immunohistochemistry was performed, which demonstrated that TNKS, β-catenin and Myc proto-oncogene protein (c-Myc) proteins are positively expressed in lung adenocarcinoma tissue; this expression was significantly higher than that in normal adjacent non-carcinoma tissues.
Using this analysis, we also revealed that five genes (TP53, EGFR, PTEN, RB1, KRAS, and CTNNB1) were somatically mutated in multiple homogeneous lung adenocarcinomas.
At the molecular level, overexpression of SH2B1 resulted in the upregulation of the EMT markers, especially induced β-catenin accumulation and activated β-catenin signaling to promote LADC cell proliferation and metastasis, while silencing SH2B1 had the opposite effect.
The present study aimed to explore the effects of Wnt/β‑catenin and Sox2 signaling on the chemoresistance of cisplatin‑resistant lung cancer cells by assessing the effects of Sox2 on Wnt/β‑catenin signaling activity, cell migration, invasion and clonogenicity, and susceptibility to cisplatin in lung adenocarcinoma A549 cells and cisplatin-resistant A549/DDP cells.
This investigation offers confirmation that PRC1 is a prognostic and promising therapeutic biomarker for people with lung adenocarcinoma and takes on a key part in the activation of the Wnt/β-catenin pathway in lung adenocarcinoma development.
Mining available gene expression data sets allowed to observe that high co-expression levels of SCD1, β-catenin, YAP/TAZ and downstream targets have a strong negative prognostic value in lung adenocarcinoma.
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.
In the present study, we demonstrated that hypoxia in lung adenocarcinoma cells can enhance Wnt signaling activity by stabilizing β-catenin and altering its localization into the nucleus.
Importantly, miR-483-5p levels are positively correlated with β-catenin expression, but are negatively correlated with the levels of RhoGDI1 and ALCAM in human lung adenocarcinoma.
Dysregulation of the canonical Wnt pathway, characterized by increased levels of β-catenin and epigenetic silencing of negative regulators, has been reported in adenocarcinoma of the lung.