Baocheng Zhu1, Hengguan Cui1, Weiqiang Xu2,3. 1. Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University, Shanghai, China. 2. Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University, Shanghai, China. xuweiqiangqp@yeah.net. 3. Qingpu Branch of Zhongshan Hospital, Fudan University, 1158 Park East Road, Qingpu District, Shanghai, 201700, China. xuweiqiangqp@yeah.net.
Abstract
BACKGROUND: Gastric cancer is one of the most prevalent and deadly malignancies without efficient treatment option. This study aimed to investigate the effect of hydrogen gas on the behavior of gastric cancer cells. METHODS: Gastric cancer cell lines MGC-803 and BGC-823 were treated with or without H2 /O2 gas mixture (66.7%:33.3% v/v). Proliferation and migration were assessed by MTT and scratch wound healing assays respectively. The expression of lncRNA MALAT1, miR-124-3p, and EZH2 was analyzed by real-time quantitative PCR and/or western blot. Tumor growth was estimated using xenograft mouse model. RESULTS: H2 gas significantly inhibited gastric tumor growth in vivo and the proliferation, migration, and lncRNA MALAT1 and EZH2 expression of gastric cancer cells while upregulated miR-124-3p expression. LncRNA MALAT1 overexpression abolished all the aforementioned effects of H2. LncRNA MALAT1 and miR-124-3p reciprocally inhibited the expression of each other. MiR-124-3p mimics abrogated lncRNA MALAT1 promoted EZH2 expression and gastric cancer cell proliferation and migration. CONCLUSIONS: These data demonstrated that H2 might be developed as a therapeutics of gastric cancer and lncRNA MALAT1/miR-124-3p/EZH2 axis could be a target for intervention.
BACKGROUND:Gastric cancer is one of the most prevalent and deadly malignancies without efficient treatment option. This study aimed to investigate the effect of hydrogen gas on the behavior of gastric cancer cells. METHODS:Gastric cancer cell lines MGC-803 and BGC-823 were treated with or without H2 /O2 gas mixture (66.7%:33.3% v/v). Proliferation and migration were assessed by MTT and scratch wound healing assays respectively. The expression of lncRNA MALAT1, miR-124-3p, and EZH2 was analyzed by real-time quantitative PCR and/or western blot. Tumor growth was estimated using xenograft mouse model. RESULTS:H2 gas significantly inhibited gastric tumor growth in vivo and the proliferation, migration, and lncRNA MALAT1 and EZH2 expression of gastric cancer cells while upregulated miR-124-3p expression. LncRNA MALAT1 overexpression abolished all the aforementioned effects of H2. LncRNA MALAT1 and miR-124-3p reciprocally inhibited the expression of each other. MiR-124-3p mimics abrogated lncRNA MALAT1 promoted EZH2 expression and gastric cancer cell proliferation and migration. CONCLUSIONS: These data demonstrated that H2 might be developed as a therapeutics of gastric cancer and lncRNA MALAT1/miR-124-3p/EZH2 axis could be a target for intervention.