Experimental energy levels of 12C14N through marvel analysis.
Ontology highlight
ABSTRACT:
SUBMITTER: Syme AM
PROVIDER: S-EPMC7545856 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The accurate choice of anti-cancer drugs is important problem of modern medicine. We developed a new method for the selection of targeted drugs based on detection of specific intracellular signaling and metabolic pathways in the bioinformatic system termed OncoFinder before the treatment. We obtained transcriptomic data 12 human cancer cell lines (NT2/D1, Tera-1, NGP, HepG2, BT474, Skov-3, T3M4, HeLa, A549, MCF-7, Jurkat, BxPc1) before a treatment. In our research for gene expression quantile normalization of the experimental data of all 12 cell lines together, we used separately eleven gene expression datasets corresponding to different normal human tissues profiled on Illumina HT-12v3-4 platform, 4-33 samples per dataset (from GEO). Normalization datasets used for the processing of the experimental transcriptomic data: GSE17822 (GSM444688, GSM444689, GSM444690, GSM444691, GSM444692, GSM444693), GSE26852 (GSM661123, GSM661124, GSM661125, GSM661126, GSM661127, GSM661128, GSM661130), GSE32124 (GSM796359, GSM796360, GSM796361, GSM796362, GSM796363, GSM796364, GSM796365, GSM796366, GSM796367, GSM796368, GSM796369, GSM796370, GSM796371, GSM796372, GSM796373, GSM796374, GSM796375, GSM796376, GSM796377, GSM796378, GSM796379, GSM796380, GSM796381, GSM796382, GSM796383, GSM796384, GSM796385, GSM796386, GSM796387, GSM796388, GSM796389, GSM796390, GSM796391), GSE34074 (GSM841415, GSM841419, GSM841423, GSM841427, GSM841431, GSM841435), GSE37013 (GSM908514, GSM908515, GSM908516, GSM908517, GSM908518, GSM908519, GSM908520), GSE40645 (GSM998797, GSM998798, GSM998799, GSM998800, GSM998801, GSM998802, GSM998803, GSM998804, GSM998805, GSM998806, GSM998807, GSM998808, GSM998809, GSM998810), GSE42656 (GSM1047460, GSM1047462, GSM1047463, GSM1047467), GSE52130 (GSM1260102, GSM1260103, GSM1260104, GSM1260105, GSM1260106, GSM1260107, GSM1260108), GSE54563 (GSM1318920, GSM1318921, GSM1318922, GSM1318923, GSM1318924, GSM1318925, GSM1318926, GSM1318927, GSM1318928, GSM1318929, GSM1318930, GSM1318931, GSM1318932, GSM1318933, GSM1318934, GSM1318935, GSM1318936, GSM1318937, GSM1318938, GSM1318939, GSM1318940, GSM1318941, GSM1318945, GSM1318946, GSM1318947), GSE57218 (GSM1380887, GSM1380888, GSM1380956, GSM1380957, GSM1380958, GSM1380959), GSE60709 (GSM1486145, GSM1486146, GSM1486160, GSM1486161, GSM1486162, GSM1486163, GSM1486164, GSM1486165, GSM1486166, GSM1486167, GSM1486168, GSM1486169, GSM1486170, GSM1486171, GSM1486172, GSM1486173). Normalization of the 12 new cell line data was performed independently 11 times together with the data from the GSM ID numbers listed above. For GSM1486145, data for replicate samples 34 and 35 were used. For sample GSM1486146, data for replicate sample 36 was used. Total RNA obtained from NT2/D1, Tera-1, NGP, HepG2, BT474, Skov-3, T3M4, HeLa, A549, MCF-7, Jurkat, BxPc1 cell lines.
2015-01-27 | E-GEOD-65314 | biostudies-arrayexpress
Project description:RNA N6 -methyladenosine (m6 A) is an emerging regulatory mechanism for tumor progression in several types of cancer. However, the underlying regulation mechanisms of m6 A methylation in colorectal cancer (CRC) remain unknown. Although the oncogenic function of methyl CpG binding protein 2 (MeCP2) has been reported, it is still unclear whether MeCP2 could alter RNA m6 A methylation state. Here, we systematically identified MeCP2 as a prometastasis gene to regulate m6 A methylation in CRC. Interestingly, MeCP2 could bind to methyltransferase-like 14 (METTL14) to coregulate tumor suppressor Kruppel-like factor 4 (KLF4) expression through changing m6 A methylation modification. Furthermore, insulin-like growth factor 2 mRNA-binding protein 2 recognized the unique modified m6 A methylation sites to enhance KLF4 mRNA stability. Taken together, these findings highlight the novel function of MeCP2 for regulating m6 A methylation and reveal the underlying molecular mechanism for the interaction between MeCP2 and METTL14, which offers a better understanding of CRC progression and metastasis.
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