| Literature DB >> 29590536 |
Yongjie Feng1, Lin Wang2, Mingyong Wang3.
Abstract
Lung cancer is the most common cause of cancer-related death. Non-small cell lung cancer (NSCLC) accounts for 80%-85% of total lung cancer cases. Dachshund homolog 1 (DACH1), is a protein encoded by the DACH1 gene in humans. DACH1 inhibits lung adenocarcinoma invasion and tumor growth but has a lower expression in NSCLC. To investigate the mechanisms of decreased DACH1 expression, its DNA methylation patterns were investigated. The results showed a higher methylation rate in NSCLC compared with the adjacent normal lung tissues. Cell transfection experiments showed that increased methylation impaired transcription factor transactivation. In vivo demethylation treatment and overexpression of DACH1 increased apoptosis and decreased migration and invasion in NSCLC A549 cells. Our research provides new insight into NSCLC pathogenesis and identifies a new therapeutic target.Entities:
Keywords: A549 cells; CPNPC; DACH1; DNA methylation; NSCLC; cellules A549; méthylation d’ADN
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Year: 2018 PMID: 29590536 DOI: 10.1139/bcb-2017-0279
Source DB: PubMed Journal: Biochem Cell Biol ISSN: 0829-8211 Impact factor: 3.626