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Environ Toxicol. 2018 Sep;33(9):955-961. doi: 10.1002/tox.22582. Epub 2018 Jul 4.

GMI, a fungal immunomodulatory protein from Ganoderma microsporum, induce apoptosis via β-catenin suppression in lung cancer cells.

Hsin IL1,2, Hsu JC1, Wu WJ1, Lu HJ3,4, Wu MF1,3,4,5, Ko JL1,3,4.

Author information

1
Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
2
Inflammation Research & Drug Development Center, Changhua Christian Hospital, Changhua, Taiwan.
3
Division of Medical Oncology, Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan.
4
School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
5
Division of Chest Medicine, Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan.

Abstract

β-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.

KEYWORDS:

GMI; apoptosis; fungal immunomodulatory protein; lung cancer; β-catenin

PMID:
29974605
DOI:
10.1002/tox.22582
[Indexed for MEDLINE]

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