{"title":"与EGFR/BRAF/KRAS野生型癌症细胞系相比,KRAS突变型肺癌癌症细胞系中的核结合蛋白-2mRNA水平下调","authors":"S. Noriaki, Imai Hisao, Okada Junichi, Yamada Eijiro, Okada Shuichi, Yamada Masanobu","doi":"10.36959/571/722","DOIUrl":null,"url":null,"abstract":"Ten of lung cancer cell lines with EGFR/BRAF/KRAS wildtype (H1299, H1819, HCC95, H838, H1437, H661, HCC15, HCC78, H1648, HCC193) and eleven of lung cancer cell lines with KRAS-mutation [KRAS-G12C (H2122, HCC44, H1792, HCC4017, H358), KRAS-G12V (H441), KRAS-G12D (HCC515), KRAS-G12R (H1264, H157), KRAS-G12A (H2009), KRAS-Q61H (H460)] were used [3]. Nucleobindin-2 mRNA level was analyzed by RT-qPCR as previously rescribed [3]. Primers and probes for Nucleobindin-2 and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) were obtained from Ori Gene Technologies (MK203097; Rockville, MD, USA;) and Applied Biosystems (Assay ID: Hs99999905_m1; Tokyo, Japan;), respectively. To normalize the amount of input cDNA, quantitative analysis was performed using the GAPDH as an internal reference. Relative expression values were computed using the comparative cycle threshold (Ct) method. All data in the figure are presented as mean ± standard deviation and were analyzed using one-way ANOVA to compare the means of all the groups. Turkey-Kramer multiple comparisons method was used to determine statistical differences between the means, with p < 0.05 deemed statistically significant using the InStat 2.00 program.","PeriodicalId":92751,"journal":{"name":"Annals of lung cancer","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Nucleobindin-2 mRNA level is down regulated in KRAS-mutation lung cancer cell lines compared with EGFR/BRAF/KRAS wild-type lung cancer cell lines\",\"authors\":\"S. Noriaki, Imai Hisao, Okada Junichi, Yamada Eijiro, Okada Shuichi, Yamada Masanobu\",\"doi\":\"10.36959/571/722\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Ten of lung cancer cell lines with EGFR/BRAF/KRAS wildtype (H1299, H1819, HCC95, H838, H1437, H661, HCC15, HCC78, H1648, HCC193) and eleven of lung cancer cell lines with KRAS-mutation [KRAS-G12C (H2122, HCC44, H1792, HCC4017, H358), KRAS-G12V (H441), KRAS-G12D (HCC515), KRAS-G12R (H1264, H157), KRAS-G12A (H2009), KRAS-Q61H (H460)] were used [3]. Nucleobindin-2 mRNA level was analyzed by RT-qPCR as previously rescribed [3]. Primers and probes for Nucleobindin-2 and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) were obtained from Ori Gene Technologies (MK203097; Rockville, MD, USA;) and Applied Biosystems (Assay ID: Hs99999905_m1; Tokyo, Japan;), respectively. To normalize the amount of input cDNA, quantitative analysis was performed using the GAPDH as an internal reference. Relative expression values were computed using the comparative cycle threshold (Ct) method. All data in the figure are presented as mean ± standard deviation and were analyzed using one-way ANOVA to compare the means of all the groups. Turkey-Kramer multiple comparisons method was used to determine statistical differences between the means, with p < 0.05 deemed statistically significant using the InStat 2.00 program.\",\"PeriodicalId\":92751,\"journal\":{\"name\":\"Annals of lung cancer\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-06-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Annals of lung cancer\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.36959/571/722\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of lung cancer","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.36959/571/722","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Nucleobindin-2 mRNA level is down regulated in KRAS-mutation lung cancer cell lines compared with EGFR/BRAF/KRAS wild-type lung cancer cell lines
Ten of lung cancer cell lines with EGFR/BRAF/KRAS wildtype (H1299, H1819, HCC95, H838, H1437, H661, HCC15, HCC78, H1648, HCC193) and eleven of lung cancer cell lines with KRAS-mutation [KRAS-G12C (H2122, HCC44, H1792, HCC4017, H358), KRAS-G12V (H441), KRAS-G12D (HCC515), KRAS-G12R (H1264, H157), KRAS-G12A (H2009), KRAS-Q61H (H460)] were used [3]. Nucleobindin-2 mRNA level was analyzed by RT-qPCR as previously rescribed [3]. Primers and probes for Nucleobindin-2 and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) were obtained from Ori Gene Technologies (MK203097; Rockville, MD, USA;) and Applied Biosystems (Assay ID: Hs99999905_m1; Tokyo, Japan;), respectively. To normalize the amount of input cDNA, quantitative analysis was performed using the GAPDH as an internal reference. Relative expression values were computed using the comparative cycle threshold (Ct) method. All data in the figure are presented as mean ± standard deviation and were analyzed using one-way ANOVA to compare the means of all the groups. Turkey-Kramer multiple comparisons method was used to determine statistical differences between the means, with p < 0.05 deemed statistically significant using the InStat 2.00 program.