Cancer Research Center, Yanbian University, Jilin, Yanbian 133002, China; Key Laboratory of the Science and Technology Department of Jilin Province, China; Key Laboratory of the Changbai Mountain, Yanbian University, Jilin, Yanbian 133002, China.
Cancer Research Center, Yanbian University, Jilin, Yanbian 133002, China; Key Laboratory of the Science and Technology Department of Jilin Province, China; Key Laboratory of the Changbai Mountain, Yanbian University, Jilin, Yanbian 133002, China.
Life Sci. 2019 Apr 15;223:110-119. doi: 10.1016/j.lfs.2019.03.025. Epub 2019 Mar 14.
Gastric cancer is a common malignancy worldwide, and is associated with high morbidity and mortality rates. Cordycepin is a 3'-deoxyadenosine drug with significant anti-cancer effects. The aim of this study was to determine the molecular mechanisms underlying cordycepin action on gastric cancer cell proliferation and migration.
The human gastric cancer cell lines MGC-803 and HGC-27 were treated with different concentrations of cordycepin (25 μM, 50 μM, 100 μM and 5 μM, 25 μM and 50 μM) for 48 h. Cell proliferation was assessed by MTT and colony formation assays, and in vitro migration by the wound healing and transwell assays. In addition, Flow Cytometry was used to detect the cell cycle and apoptosis. RT-PCR and Western blotting were used to evaluate the expression levels of key factors.
Cordycepin significantly inhibited gastric cancer cell proliferation and migration in a dose-dependent manner, in addition to inducing apoptosis and arresting the cell cycle at the G2 phase. Mechanistically, cordycepin targeted the PI3K/Akt signaling pathway by significantly altering the expression levels/activation of several key mediators, and upregulated the anti-metastatic factor CLEC2.
Cordycepin inhibited the proliferation and migration of gastric cancer cells by upregulating CLEC2 via the Akt signaling pathway.
胃癌是一种常见的全球恶性肿瘤，与高发病率和死亡率相关。虫草素是一种具有显著抗癌作用的 3'-脱氧腺苷药物。本研究旨在确定虫草素对胃癌细胞增殖和迁移作用的分子机制。
用不同浓度的虫草素（25μM、50μM、100μM 和 5μM、25μM 和 50μM）处理人胃癌细胞系 MGC-803 和 HGC-27 48h。通过 MTT 和集落形成实验评估细胞增殖，通过划痕愈合和 Transwell 实验评估体外迁移。此外，流式细胞术用于检测细胞周期和凋亡。RT-PCR 和 Western blot 用于评估关键因子的表达水平。
虫草素呈剂量依赖性显著抑制胃癌细胞的增殖和迁移，同时诱导细胞凋亡并将细胞周期阻滞在 G2 期。在机制上，虫草素通过显著改变几个关键介质的表达水平/激活来靶向 PI3K/Akt 信号通路，并上调抗转移因子 CLEC2。
虫草素通过 Akt 信号通路上调 CLEC2 抑制胃癌细胞的增殖和迁移。
