{"title":"金丝桃苷通过NF-κB/PTEN/JAK2通路促进胃癌细胞凋亡及抑制细胞活力","authors":"Bo Shu","doi":"10.31901/24566330.2022/22.03.819","DOIUrl":null,"url":null,"abstract":"This study investigated impacts of hyperoside on viabilities and apoptosis of gastric cancer (GC) cells. CCK-8 and flow cytometry were applied for examining HGC-27 cell viabilities and apoptosis, indicating that hyperoside treatment suppressed cell viabilities but facilitated cell apoptosis. Additionally, RT-qPCR results revealed that mRNA expressions of Bcl-2 in HGC-27 cells were downregulated while Bax and caspase-3 were elevated with hyperoside treatment. Furthermore, ELISA examined changes about protein concentrations of NF-κB/PTEN/JAK signalling pathway in HGC-27 cells after being treated by hyperoside. Results showed that protein concentrations of phosphorylated NF-κB/ p65 were reduced with hyperoside treatment while PTEN and JAK2 protein concentrations were promoted.","PeriodicalId":0,"journal":{"name":"","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Hyperoside Facilitates Gastric Cancer (GC) Cell Apoptosis and Inhibits Viability via NF-κB/PTEN/JAK2 Pathway\",\"authors\":\"Bo Shu\",\"doi\":\"10.31901/24566330.2022/22.03.819\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"This study investigated impacts of hyperoside on viabilities and apoptosis of gastric cancer (GC) cells. CCK-8 and flow cytometry were applied for examining HGC-27 cell viabilities and apoptosis, indicating that hyperoside treatment suppressed cell viabilities but facilitated cell apoptosis. Additionally, RT-qPCR results revealed that mRNA expressions of Bcl-2 in HGC-27 cells were downregulated while Bax and caspase-3 were elevated with hyperoside treatment. Furthermore, ELISA examined changes about protein concentrations of NF-κB/PTEN/JAK signalling pathway in HGC-27 cells after being treated by hyperoside. Results showed that protein concentrations of phosphorylated NF-κB/ p65 were reduced with hyperoside treatment while PTEN and JAK2 protein concentrations were promoted.\",\"PeriodicalId\":0,\"journal\":{\"name\":\"\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0,\"publicationDate\":\"2022-06-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.31901/24566330.2022/22.03.819\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.31901/24566330.2022/22.03.819","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Hyperoside Facilitates Gastric Cancer (GC) Cell Apoptosis and Inhibits Viability via NF-κB/PTEN/JAK2 Pathway
This study investigated impacts of hyperoside on viabilities and apoptosis of gastric cancer (GC) cells. CCK-8 and flow cytometry were applied for examining HGC-27 cell viabilities and apoptosis, indicating that hyperoside treatment suppressed cell viabilities but facilitated cell apoptosis. Additionally, RT-qPCR results revealed that mRNA expressions of Bcl-2 in HGC-27 cells were downregulated while Bax and caspase-3 were elevated with hyperoside treatment. Furthermore, ELISA examined changes about protein concentrations of NF-κB/PTEN/JAK signalling pathway in HGC-27 cells after being treated by hyperoside. Results showed that protein concentrations of phosphorylated NF-κB/ p65 were reduced with hyperoside treatment while PTEN and JAK2 protein concentrations were promoted.