WEN-JUN WUHSUEH-JU LUJIUNN-LIANG KO2026-10-162026-10-162018-09-01Pure ID: 15139056Pure UUID: 2367e90f-d069-45f6-84af-fece2fe94a8a10.1002/tox.22582https://www.scopus.com/pages/publications/85050807662https://scholars.csmu.edu.tw/handle/123456789/28264β-catenin is important in development of lung cancer. In our previous study, GMI, a fungal immunomodulatory protein, inhibits lung cancer cell survival. The aim of this study is to evaluate the effect of GMI on β-catenin inhibition and apoptosis induction. GMI induced apoptosis in lung cancer cells bearing wild-type and mutated EGFR. GMI did not reduce the β-catenin mRNA expression but suppressed the protein expressions of β-catenin that resulted in the transcriptional downregulation of its target genes: survivin and cyclin-D1. The transcriptional activation activity of β-catenin was demonstrated by TOPFLASH/FOPFLASH luciferase reporter assay. Inhibition of GSK-3β and proteasome blocked the inhibiting effect of GMI on β-catenin and its target genes. β-catenin silencing increased activation of apoptosis in GMI-treated H1355 cells. This is the first study to reveal the novel function of GMI in inducing apoptosis via β-catenin inhibition. These results provide a new potential of GMI in against lung cancer.7enjournal article