AT-rich interactive domain1A determines sensitivity to oxaliplatin in gastric cancer cells

• Published in: Translational cancer research Vol. 9; no. 12; pp. 7540 - 7549
• Main Authors: Liu, Qing, Weng, Qing-Qing, Shen, Song-Fei, Jiang, Tao, Pan, Zhang-Chi, Lin, Meng-Xin, Lan, Yan-Qin, Wang, Yao, Chen, Qiang, Shi, Chun-Mei
• Format: Journal Article
• Language: English
• Published: China AME Publishing Company 01.12.2020
• Subjects: Original; gastric cancer; AT-rich interactive domain1A (ARID1A); oxaliplatin
• ISSN: 2218-676X; 2219-6803
• DOI: 10.21037/tcr-20-2384

Gastric cancer is a highly heterogeneous disease and its traditional histopathological classification is difficult to meet clinical needs. Oxaliplatin is an antitumor drug with high efficiency and low toxicity. Therefore, the insensitivity or secondary drug resistance of oxaliplatin to gastric cancer is vital for tumor progression. The aim of this study was to investigate the sensitivity of gastric cancer cells to oxaliplatin after (AT-rich interactive domain1A gene) gene silencing. MGC-803 and AGS cells were selected as gastric cancer cells for study. ARID1A protein and mRNA expression was detected by Western blot and quantitative reverse-transcription PCR (qRT-PCR). The short hairpin RNA (shRNA) fragment of gene silencing was constructed and introduced into gastric cancer cells. The cell proliferation activity was calculated using CCK8 and the IC50 was calculated. The flow cytometry was used to detect the cell cycle and apoptosis rate. The ability of cell invasion was detected by transwell method. Cells were treated with different concentrations of oxaliplatin. The proliferation of gastric cancer cells was promoted by gene silencing (P<0.01), the quantity of cells in S phase increased (P<0.05), and the invasive ability increased (P<0.05). After treatment with oxaliplatin at different concentrations, gene silencing reduced the inhibition rate of oxaliplatin on gastric cancer cells and apoptosis rate (P<0.05), and increased IC 50 (P<0.01). gene silencing, a factor promoting proliferation of gastric cancer cells, would reduce the sensitivity of gastric cancer cells to oxaliplatin, which can provide a basis for the exploration of targeted drugs for individualized treatment of gastric cancer.