Alteration ofDACH1methylation patterns in lung cancer contributes to cell proliferation and migration

Author:

Feng Yongjie1,Wang Lin2,Wang Mingyong3

Affiliation:

1. School of Biology & Basic Medical Science, Soochow University, Suzhou 215123, P.R. China.

2. Department of JiNan Children’s Hospital, Jinan, 250022, P.R. China.

3. College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu 215021, P.R. China.

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.

Publisher

Canadian Science Publishing

Subject

Cell Biology,Molecular Biology,Biochemistry

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