Association between the ATF3 gene and non‐small cell lung cancer

Thoracic Cancer

Xiaoxue Song¹  Fang Lu¹  Reng-Yun Liu¹  Zhe Lei¹  Jun Zhao³  Qinghua Zhou² 

[1] Soochow University Laboratory of Cancer Molecular Genetics, Medical College of Soochow University, Suzhou, China;Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University, Tianjin, China;Department of Thoraco-cardiac Surgery, The First Affiliated Hospital, Soochow University, Suzhou, China

关键词: NSCLC;    ATF3;    mutation;    methylation;    risk;   

DOI  :  10.1111/j.1759-7714.2011.00110.x

来源: Wiley

【 摘 要 】

Abstract

Background:  Non-small cell lung cancer (NSCLC) accounts for ∼85% of all cases of lung cancer and has a poor prognosis. Activating transcription factor 3 (ATF3), a member of the ATF/cyclic adenosine monophosphate response element binding (ATF/cyclic response element binding) family of transcription factors, has been implicated in the pathogenesis of several types of cancer. However, whether the expression of ATF3 is aberrant in NSCLC and genetic variants, or DNA methylation of the gene contributes to the tumorigenesis of NSCLC, are largely unknown.

Methods:  The expression of ATF3 in four NSCLC cell lines and normal human bronchial epithelial cell (HBEpiC) line was detected by Western blot analysis. The mutation of the 5′-flanking 1500-bp and coding sequence regions of the ATF3 gene were screened using DNA direct sequencing, and bisulfite-sodium modification sequencing was used to detect the promoter methylation status of the gene.

Results:  up-regulated expression of ATF3 was observed in NSCLC cell lines, and there was no difference in the sequence regions of the ATF3 gene between NSCLC cells and HBEpiC cells, which were validated in lung cancer tissues and their corresponding paracarcinoma tissues.

Conclusion:  Our findings suggest that the tumorigenesis of NSCLC may particularly attribute to increased expression of ATF3 but not the genetic variants of the gene.

【 授权许可】

Unknown   
© 2012 Tianjin Lung Cancer Institute and Blackwell Publishing Asia Pty. Ltd