{"title":"FGF1信号通过激活极光激酶调节胶质母细胞瘤干细胞的自我更新","authors":"Chien-Yu Kao, Yi-Chao Hsu, I. Chiu","doi":"10.14800/CCM.1389","DOIUrl":null,"url":null,"abstract":"Glioblastoma (GBM) is a highly malignant brain tumor. The GBM tumor mass contains a unique cell population, GBM stem cells (GBM-SCs), which possess the self-renewal, tumor initiating and tumor progression. FGF1B is the major transcriptional variant of FGF1 in GBM. In our recent study, we demonstrated the FGF1B transcript is up-regulated in self-renewing GBM cells. In order to study GBM-SCs, we developed an approach to isolate GBM-SCs by using FGF1B promoter-driven GFP reporter (F1BGFP). We showed that F1BGFP(+) GBM cells exhibit higher phosphorylation levels of FGFR and AurA than F1BGFP(-) cells, indicating the activation of FGFR and AurA. In this research highlight, we summarized the role of FGF1 signaling and AurA in tumorigenesis. In addition, we also suggested that FGF1-FGFR-AurA cascade regulates GBM-SCs, which may enable development of target-based therapy that act against the GBM-SCs.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"80 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2016-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"FGF1 signaling regulates self-renewal of glioblastoma stem cells through activation of aurora a kinase\",\"authors\":\"Chien-Yu Kao, Yi-Chao Hsu, I. Chiu\",\"doi\":\"10.14800/CCM.1389\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Glioblastoma (GBM) is a highly malignant brain tumor. The GBM tumor mass contains a unique cell population, GBM stem cells (GBM-SCs), which possess the self-renewal, tumor initiating and tumor progression. FGF1B is the major transcriptional variant of FGF1 in GBM. In our recent study, we demonstrated the FGF1B transcript is up-regulated in self-renewing GBM cells. In order to study GBM-SCs, we developed an approach to isolate GBM-SCs by using FGF1B promoter-driven GFP reporter (F1BGFP). We showed that F1BGFP(+) GBM cells exhibit higher phosphorylation levels of FGFR and AurA than F1BGFP(-) cells, indicating the activation of FGFR and AurA. In this research highlight, we summarized the role of FGF1 signaling and AurA in tumorigenesis. In addition, we also suggested that FGF1-FGFR-AurA cascade regulates GBM-SCs, which may enable development of target-based therapy that act against the GBM-SCs.\",\"PeriodicalId\":9576,\"journal\":{\"name\":\"Cancer cell & microenvironment\",\"volume\":\"80 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2016-08-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cancer cell & microenvironment\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.14800/CCM.1389\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer cell & microenvironment","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14800/CCM.1389","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
FGF1 signaling regulates self-renewal of glioblastoma stem cells through activation of aurora a kinase
Glioblastoma (GBM) is a highly malignant brain tumor. The GBM tumor mass contains a unique cell population, GBM stem cells (GBM-SCs), which possess the self-renewal, tumor initiating and tumor progression. FGF1B is the major transcriptional variant of FGF1 in GBM. In our recent study, we demonstrated the FGF1B transcript is up-regulated in self-renewing GBM cells. In order to study GBM-SCs, we developed an approach to isolate GBM-SCs by using FGF1B promoter-driven GFP reporter (F1BGFP). We showed that F1BGFP(+) GBM cells exhibit higher phosphorylation levels of FGFR and AurA than F1BGFP(-) cells, indicating the activation of FGFR and AurA. In this research highlight, we summarized the role of FGF1 signaling and AurA in tumorigenesis. In addition, we also suggested that FGF1-FGFR-AurA cascade regulates GBM-SCs, which may enable development of target-based therapy that act against the GBM-SCs.