血管生成
小RNA
上皮-间质转换
下调和上调
化学
癌症研究
癌症
转染
癌细胞
分子生物学
生物
医学
生物化学
内科学
基因
作者
Wei Liu,Han Chen,Dongsheng Wang
标识
DOI:10.1080/08923973.2021.1936013
摘要
AIM: Astragaloside IV (AS-IV) was reported to exert anti-cancer function in many cancers, but its actions in gastric cancer (GC) remain unclear. In the present study, we tried to elaborate the underlying mechanism by which AS-IV regulated the epithelial-mesenchymal transition (EMT) and angiogenesis of GC cells. METHODS: The expressions of hsa-miR-15b-5p, hsa-miR-15a-5p, hsa-miR-195-5p, hsa-miR-424-5p and hsa-miR-497-5p in GC tissues and adjacent normal tissues were predicted by TCGA database. SGC7901 or MGC803 cells were treated with AS-IV, or transfected with miR-195-5p inhibitor/mimic or pcDNA3.1-PD-L1 followed by detection of cell proliferation, EMT and angiogenesis. The target relation between miR-195-5p and PD-L1 was confirmed by dual luciferase reporter gene assay. RESULTS: Elevated hsa-miR-15b-5p, hsa-miR-15a-5p and hsa-miR-424-5p expressions were found in GC tissues, while decreased hsa-miR-195-5p and hsa-miR-497-5p expressions were observed in GC tissues. AS-IV inhibits EMT and angiogenesis in GC. PD-L1 was a potential target of miR-195-5p. Down-regulation of miR-195-5p or elevated PD-L1 expression reverses the inhibitory effect of AS-IV on EMT and angiogenesis of GC cells. CONCLUSION: miR-195-5p-regulated PD-L1.
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