Research Article

Tumor Biology

, Volume 35, Issue 6, pp 5701-5707

ARID1A is downregulated in non-small cell lung cancer and regulates cell proliferation and apoptosis

  • Yi ZhangAffiliated withDepartment of Geriatrics, Shengjing Hospital of China Medical University
  • , Xiaoman XuAffiliated withDepartment of Respiratory Medicine, Shengjing Hospital of China Medical University
  • , Meng ZhangAffiliated withDepartment of Geriatrics, Shengjing Hospital of China Medical University
  • , Xue BaiAffiliated withDepartment of Geriatrics, Shengjing Hospital of China Medical University
  • , Hui LiAffiliated withDepartment of Geriatrics, Shengjing Hospital of China Medical University
  • , Liang KanAffiliated withDepartment of Geriatrics, Shengjing Hospital of China Medical University
  • , Huiyan NiuAffiliated withDepartment of Geriatrics, Shengjing Hospital of China Medical University
  • , Ping HeAffiliated withDepartment of Geriatrics, Shengjing Hospital of China Medical University Email author 

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Abstract

ARID1A (AT-rich interactive domain 1A) is a key member of the SWI/SNF chromatin-modeling complex, and the gene has emerged as a tumor suppressor in various human cancers. In the present study, we investigated the expression and clinical significance of ARID1A in non-small cell lung cancer (NSCLC). We found that ARID1A expression was decreased in NSCLC tissues compared with normal bronchial epithelium and was significantly correlated with nodal metastasis, tumor, node, metastasis (TNM) stage, and poor differentiation. ARID1A expression was lower in lung cancer cell lines than normal bronchial epithelial HBE cell line. We also explored the involvement of ARID1A in biological behavior of lung cancer cell lines. ARID1A depletion by small interfering RNA (siRNA) in H460 and H1299 cell lines promoted proliferation, colony formation ability, and inhibited paclitaxel-induced apoptosis. Furthermore, we identified that ARID1A regulated several cell cycle and apoptosis-related targets such as cyclin D1 and Bcl-2. In addition, the activity of Akt phosphorylation was also enhanced after ARID1A depletion. In conclusion, our data suggested that ARID1A may serve as an important tumor suppressor in NSCLC.

Keywords

ARID1A Non-small cell lung cancer Proliferation Apoptosis