Liu Xiaoqian, Ju Jianfeng, Liu Qun, Zhu Zongmin, Liu Chunxia
Department of Pharmacy, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250011, Shandong, People's Republic of China.
Department of Pharmacy, Caoxian People's Hospital of Heze City, Heze 274400, Shandong, People's Republic of China.
Cancer Manag Res. 2020 Jul 13;12:5677-5687. doi: 10.2147/CMAR.S242856. eCollection 2020.
In recent years, traditional Chinese medicine has achieved good results in treating gliomas. This research aimed to reveal the effect of Shezhi Huangling decoction (SD) on glioma cell process.
U87 and U251 cells were treated with different concentrations (10, 30 and 50 μg/mL) of SD or transfected with miR-1298-5p mimic, inhibitor and siRNA targeting TGIF1. Cell proliferation, migration, invasion and apoptosis were detected. The expression of miR-1298-5p was measured by qRT-PCR, while TGIF1 expression was examined by immunohistochemical analysis and Western blot.
SD treatment inhibited the proliferation, migration and invasion of glioma cells and induced the apoptosis. In addition, SD treatment induced the expression of miR-1298-5p in glioma cells. The low expression of miR-1298-5p was examined in glioma tissues and was significantly related to the high histological grade of glioma patients and predicted a poor prognosis. MiR-1298-5p directly targeted the 3'-UTR of transforming growth factor β induced factor 1 (TGIF1) and reduced TGIF1 protein expression. MiR-1298-5p restricted the proliferation, migration and invasion of glioma cells and induced cell apoptosis by targeting TGIF1.
Our data reveal that SD acts as a cancer-inhibiting agent in glioma via miR-1298-5p/TGIF1 axis, suggesting a potential therapeutic application of SD in glioma.
近年来,中药在治疗胶质瘤方面取得了良好效果。本研究旨在揭示蛇蛭黄灵汤(SD)对胶质瘤细胞进程的影响。
用不同浓度(10、30和50μg/mL)的SD处理U87和U251细胞,或用miR-1298-5p模拟物、抑制剂和靶向TGIF1的小干扰RNA(siRNA)转染细胞。检测细胞增殖、迁移、侵袭和凋亡情况。通过qRT-PCR检测miR-1298-5p的表达,通过免疫组织化学分析和蛋白质印迹法检测TGIF1的表达。
SD处理抑制了胶质瘤细胞的增殖、迁移和侵袭,并诱导了细胞凋亡。此外,SD处理诱导了胶质瘤细胞中miR-1298-5p的表达。在胶质瘤组织中检测到miR-1298-5p低表达,且与胶质瘤患者的高组织学分级显著相关,并预示预后不良。miR-1298-5p直接靶向转化生长因子β诱导因子1(TGIF1)的3'-非翻译区(3'-UTR),降低TGIF1蛋白表达。miR-1298-5p通过靶向TGIF1限制了胶质瘤细胞的增殖、迁移和侵袭,并诱导细胞凋亡。
我们的数据表明,SD通过miR-1298-5p/TGIF1轴在胶质瘤中发挥抗癌作用,提示SD在胶质瘤中具有潜在的治疗应用价值。