{"title":"微小RNA-184通过PI3K/AKT/mTOR增加癌症对顺铂的耐药性","authors":"S. Ding, Keli Zhong, Kaibin Huang, Ligang Xia","doi":"10.1166/jbt.2023.2624","DOIUrl":null,"url":null,"abstract":"This study sought for investigating the function of miR-184 in resistance of gastric cancer (GC) cells to cisplatin (DDP). Consequently, not only BGC-823 DDP-resistant GC cells (BGC-823/DDP) but also SGC-7901 DDP-resistant cells (SGC-7901/DDP) were upregulated in contrast with their\n parent cells. Ectopic expressed miR-184 mimetics increased DDP resistance and increased migration as well as invasion in cisplatin-resistant cells. Nevertheless, miR-184 inhibitors reduced DDP resistance, cell invasion as well as migration in parent cells. Besides, Ncor2 is a direct targeting\n gene for miR-184 in GC cells. Ncor2 gene knockout revealed that DDP resistance promoted cisplatin-resistant cells. Conversely, over Ncor2 expression in BGC-823 cells generated the effect of suppressing resistance to cisplatin. Additionally, over miR-184 expression raised the resistance of\n cisplatin-resistant cells to DDP, in part arise from the activation of the Ncor2/PI3K/AKT/mTOR signal pathway. miR-184 could also lessen the sensitivity of BGC-823/DDP cells to cisplatin in vivo. To conclude, we evidence that the inactivation of miR-184 or the activation of channel\n of its target gene can be served as an innovation to reverse DDP resistance in GC.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1000,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"MicroRNA-184 Increases the Resistance of Gastric Cancer to Cisplatin via PI3K/AKT/mTOR\",\"authors\":\"S. Ding, Keli Zhong, Kaibin Huang, Ligang Xia\",\"doi\":\"10.1166/jbt.2023.2624\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"This study sought for investigating the function of miR-184 in resistance of gastric cancer (GC) cells to cisplatin (DDP). Consequently, not only BGC-823 DDP-resistant GC cells (BGC-823/DDP) but also SGC-7901 DDP-resistant cells (SGC-7901/DDP) were upregulated in contrast with their\\n parent cells. Ectopic expressed miR-184 mimetics increased DDP resistance and increased migration as well as invasion in cisplatin-resistant cells. Nevertheless, miR-184 inhibitors reduced DDP resistance, cell invasion as well as migration in parent cells. Besides, Ncor2 is a direct targeting\\n gene for miR-184 in GC cells. Ncor2 gene knockout revealed that DDP resistance promoted cisplatin-resistant cells. Conversely, over Ncor2 expression in BGC-823 cells generated the effect of suppressing resistance to cisplatin. Additionally, over miR-184 expression raised the resistance of\\n cisplatin-resistant cells to DDP, in part arise from the activation of the Ncor2/PI3K/AKT/mTOR signal pathway. miR-184 could also lessen the sensitivity of BGC-823/DDP cells to cisplatin in vivo. To conclude, we evidence that the inactivation of miR-184 or the activation of channel\\n of its target gene can be served as an innovation to reverse DDP resistance in GC.\",\"PeriodicalId\":15300,\"journal\":{\"name\":\"Journal of Biomaterials and Tissue Engineering\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.1000,\"publicationDate\":\"2023-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Biomaterials and Tissue Engineering\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1166/jbt.2023.2624\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biomaterials and Tissue Engineering","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1166/jbt.2023.2624","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
MicroRNA-184 Increases the Resistance of Gastric Cancer to Cisplatin via PI3K/AKT/mTOR
This study sought for investigating the function of miR-184 in resistance of gastric cancer (GC) cells to cisplatin (DDP). Consequently, not only BGC-823 DDP-resistant GC cells (BGC-823/DDP) but also SGC-7901 DDP-resistant cells (SGC-7901/DDP) were upregulated in contrast with their
parent cells. Ectopic expressed miR-184 mimetics increased DDP resistance and increased migration as well as invasion in cisplatin-resistant cells. Nevertheless, miR-184 inhibitors reduced DDP resistance, cell invasion as well as migration in parent cells. Besides, Ncor2 is a direct targeting
gene for miR-184 in GC cells. Ncor2 gene knockout revealed that DDP resistance promoted cisplatin-resistant cells. Conversely, over Ncor2 expression in BGC-823 cells generated the effect of suppressing resistance to cisplatin. Additionally, over miR-184 expression raised the resistance of
cisplatin-resistant cells to DDP, in part arise from the activation of the Ncor2/PI3K/AKT/mTOR signal pathway. miR-184 could also lessen the sensitivity of BGC-823/DDP cells to cisplatin in vivo. To conclude, we evidence that the inactivation of miR-184 or the activation of channel
of its target gene can be served as an innovation to reverse DDP resistance in GC.