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

• Published in: Tumor biology Vol. 35; no. 6; pp. 5701 - 5707
• Main Authors: Zhang, Yi, Xu, Xiaoman, Zhang, Meng, Bai, Xue, Li, Hui, Kan, Liang, Niu, Huiyan, He, Ping
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer Netherlands 01-06-2014; Springer Nature B.V
• Subjects: Adult; Aged; Apoptosis; Biomedical and Life Sciences; Biomedicine; Cancer Research; Carcinoma, Non-Small-Cell Lung - drug therapy; Carcinoma, Non-Small-Cell Lung - mortality; Carcinoma, Non-Small-Cell Lung - pathology; Cell Proliferation; Cellular biology; Cyclin D1 - metabolism; Down-Regulation; Female; Gene expression; Humans; Lung cancer; Lung Neoplasms - drug therapy; Lung Neoplasms - mortality; Lung Neoplasms - pathology; Male; Middle Aged; Nuclear Proteins - analysis; Nuclear Proteins - physiology; Phosphorylation; Proto-Oncogene Proteins c-akt - metabolism; Research Article; Transcription Factors - analysis; Transcription Factors - physiology; Tumor Suppressor Proteins - physiology; Proliferation; ARID1A; Non-small cell lung cancer; Apoptosis
• ISSN: 1010-4283; 1423-0380
• DOI: 10.1007/s13277-014-1755-x

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.