Literature DB >> 28746919

C/EBPα Suppresses Lung Adenocarcinoma Cell Invasion and Migration by Inhibiting β-Catenin.

Jinchang Lu1, Chunling Du1, Junxia Yao2, Bo Wu1, Yanhong Duan1, Lei Zhou1, Donghui Xu1, Feng Zhou1, Liang Gu1, Hong Zhou1, Yingxin Sun1.   

Abstract

BACKGROUND/AIMS: The transcription factor CCAAT/enhancer-binding protein α (C/EBPα) is a basic leucine zipper transcription factor that plays essential roles in tumor progression. Although decreased or absent C/EBPα expression in many cancers suggests a possible role for C/EBPα as a tumor suppressor, the functions of C/EBPα in lung adenocarcinoma remain unclear.
METHODS: Here, C/EBPα expression levels in 26 lung adenocarcinoma and para-carcinoma tissue samples were detected by qRT-PCR and immunohistochemistry. Cell transwell assays, wound healing assay and three-dimensional spheroid invasion assay were performed to assess the effects of C/EBPα on migration and invasion in lung adenocarcinoma cells in vitro. Western blotting was applied to analyze the potential mechanisms.
RESULTS: C/EBPα was found to be decreased in lung adenocarcinoma tissues compared to para-carcinoma tissues. Overexpression of C/EBPα significantly inhibited the migration and invasion of lung adenocarcinoma cells. In addition, C/EBPα overexpression suppressed the epithelial-mesenchymal transition (EMT) that was characterized by a gain of epithelial and loss of mesenchymal markers. Further study showed that C/EBPα suppressed the transcription of β-catenin and downregulated the levels of its downstream targets.
CONCLUSION: Our data suggest that C/EBPα inhibits lung adenocarcinoma cell invasion and migration by suppressing β-catenin-mediated EMT in vitro. Thus, C/EBPα may be helpful as a potential target for treatment of lung adenocarcinoma.
© 2017 The Author(s). Published by S. Karger AG, Basel.

Entities:  

Keywords:  C/EBPα; Invasion; Lung adenocarcinoma; Migration; β-catenin

Mesh:

Substances:

Year:  2017        PMID: 28746919     DOI: 10.1159/000479457

Source DB:  PubMed          Journal:  Cell Physiol Biochem        ISSN: 1015-8987


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