Transcriptomic analysis of neuroblastoma cells in response to stable over-expression of armadillo repeat containing 12 (ARMC12)
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ABSTRACT:
PROVIDER: PRJNA420394 | ENA |
REPOSITORIES: ENA
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Project description:Neuroblastoma (NB), a malignant embryonic tumor arising from primitive neural crest cells, accounts for more than 7% of malignancies and around 15% of cancer-related mortality in childhood. Better elucidating the mechanisms of tumorigenesis and aggressiveness is important for improving the therapeutic efficiencies of NB. Through mining of a public microarray dataset, we identified armadillo repeat containing 12 (ARMC12) as a novel ARM member associated with the progression of NB. To investigate the mechanisms underlying the oncogenic functions of ARMC12, we employed the Illumina HiSeq X Ten as a discovery platform to analyze the transcriptome profiling changes of human SH-SY5Y cells in response to stable over-expression of ARMC12. The results showed that stable over-expression of ARMC12 led to altered expression of 6125 human mRNAs, including 2901 up-regulated genes and 3224 down-regulated genes. Then we found the possible roles of these differentially regulated mRNAs in selected pathways including cell cycle/proliferation, invasion, and metastasis by bioinformatic analysis. Furthermore, we validated the RNA-seq results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to ARMC12 over-expression in human NB cells, and these findings will help us understand the pathogenesis of NB.
2018-11-30 | GSE107516 | GEO
Project description:Cellular nucleic acid binding protein (CNBP) is a 19 kDa conserved protein containing seven tandem cysteine-cysteine-histidine-cysteine zinc finger repeats. However, the action modes and underlying mechanisms of CNBP in NB progression remain largely unknown. We identify CNBP as an independent prognostic factor for poor outcome of neuroblastoma. CNBP exerts oncogenic roles in ribosome biogenesis, tumorigenesis, and aggressiveness. To investigate the mechanisms underlying the oncogenic functions of CNBP, we employed the Illumina HiSeq X Ten as a discovery platform to analyze the transcriptome profiling changes of human neuroblastoma IMR-32 cells in response to stable over-expression of CNBP. The results showed that stable over-expression of CNBP led to altered expression of 3524 human mRNAs, including 889 up-regulated genes and 2635 down-regulated genes. Furthermore, we validated the RNA-seq results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to CNBP over-expression in human tumor cells, and these findings will help us understand the pathogenesis of tumor progression.
2023-05-03 | GSE215748 | GEO
Project description:Neuroblastoma is the most common extracranial solid malignancy derived from neural crest cells. Better elucidation of the mechanisms underlying the aggressive progression of neuroblastoma is needed for improving the therapeutic efficiencies. Since previous studies indicate that histone H2A type 2-B (H2AB), a histone H2A variant locating at chromosome 1q21.2 region, is up-regulated in neural progenitor cells and early motor neurons, we hypothesized that H2AB might participate in the progression of neuroblastoma. We employed the human whole genome microarray expression profiling as a discovery platform to analyze the transcriptome profiling changes of human neuroblastoma SH-SY5Y cells in response to stable over-expression of H2AB. The results showed that stable over-expression of H2AB led to altered expression of 514 human mRNAs, including 249 up-regulated genes and 265 down-regulated genes. Then we found the possible roles of these differentially regulated mRNAs in selected pathways including cell cycle/proliferation, apoptosis, and cytokine/chemokine responses by Bioinformatic analysis. Furthermore, we validated the microarray results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to H2AB over-expression in human neuroblastoma cells, and these findings will help us to understand the pathogenesis of neuroblastoma.
2014-07-01 | GSE52852 | GEO
Project description:Neuroblastoma is the most common extracranial solid malignancy derived from neural crest cells. Better elucidation of the mechanisms underlying the aggressive progression of neuroblastoma is needed for improving the therapeutic efficiencies. Since previous studies indicate that histone H2A type 2-B (H2AB), a histone H2A variant locating at chromosome 1q21.2 region, is up-regulated in neural progenitor cells and early motor neurons, we hypothesized that H2AB might participate in the progression of neuroblastoma. We employed the human whole genome microarray expression profiling as a discovery platform to analyze the transcriptome profiling changes of human neuroblastoma SH-SY5Y cells in response to stable over-expression of H2AB. The results showed that stable over-expression of H2AB led to altered expression of 514 human mRNAs, including 249 up-regulated genes and 265 down-regulated genes. Then we found the possible roles of these differentially regulated mRNAs in selected pathways including cell cycle/proliferation, apoptosis, and cytokine/chemokine responses by Bioinformatic analysis. Furthermore, we validated the microarray results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to H2AB over-expression in human neuroblastoma cells, and these findings will help us to understand the pathogenesis of neuroblastoma. Total RNA of cells stably transfected with empty vector or H2AB was extracted using the TRIZOL Reagent according to the manufacturer's instructions. Gene expression profiling was performed for each RNA sample separately on the Agilent Whole Human Genome Oligo Microarray 4M-CM-^W44K at Shanghai Technology Corporation (Shanghai, China), in which GeneChip microarray service was certificated by Agilent.
2014-07-01 | E-GEOD-52852 | biostudies-arrayexpress
Project description:Long noncoding RNAs (lncRNAs), one type of endogenous RNA longer than 200 nucleotides, play emerging roles in tumorigenesis and aggressiveness. However, the functions and underlying mechanisms of lncRNAs in regulating neuroblastoma progression still remain elusive. We identify GATA2 antisense RNA 1 (GATA2-AS1), a lncRNA derived from GATA binding protein 2 (GATA2), as a novel suppressor of neuroblastoma progression. To investigate the mechanisms underlying the oncogenic functions of GATA2-AS1, we employed the Illumina HiSeq X Ten as a discovery platform to analyze the transcriptome profiling changes of human neuroblastoma BE(2)-C cells in response to stable over-expression of GATA2-AS1. The results showed that stable over-expression of GATA2-AS1 led to altered expression of 1933 human mRNAs, including 857 up-regulated genes and 1076 down-regulated genes. Furthermore, we validated the RNA-seq results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to GATA2-AS1 over-expression in human tumor cells, and these findings will help us understand the pathogenesis of tumor progression.
2024-04-15 | GSE229665 | GEO
Project description:Neuroblastoma (NB), a malignant embryonic tumor arising from primitive neural crest cells, accounts for more than 7% of malignancies and around 15% of cancer-related mortality in childhood. Better elucidating the mechanisms of tumorigenesis and aggressiveness is important for improving the therapeutic efficiencies of NB. Through mining public microarray and RNA sequencing datasets, we identified neuroblastoma highly expressed 1 (NHEG1) as a novel 1360-bp lncRNA associated with poor outcome of NB. To investigate the mechanisms underlying the oncogenic functions of NHEG1, we employed the human whole genome microarray expression profiling as a discovery platform to analyze the transcriptome profiling changes of human SH-SY5Y cells in response to stable over-expression of NHEG1. The results showed that stable over-expression of NHEG1 led to altered expression of 869 human mRNAs, including 499 up-regulated genes and 370 down-regulated genes. Then we found the possible roles of these differentially regulated mRNAs in selected pathways including cell cycle/proliferation, apoptosis, and cytokine/chemokine responses by Bioinformatic analysis. Furthermore, we validated the microarray results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to NHEG1 over-expression in human NB cells, and these findings will help us understand the pathogenesis of NB.
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Project description:Circular RNAs (circRNAs), a subclass of noncoding RNAs characterized by covalently closed continuous loops, play emerging roles in tumorigenesis and aggressiveness. However, the functions and underlying mechanisms of circRNAs in regulating neuroblastoma progression still remain elusive. We identify one circRNA derived from CUX1 (circ-CUX1) as a novel driver of neuroblastoma progression. To investigate the mechanisms underlying the oncogenic functions of circ-CUX1, we employed the Illumina HiSeq X Ten as a discovery platform to analyze the transcriptome profiling changes of human neuroblastoma IMR32 cells in response to stable over-expression of circ-CUX1. The results showed that stable over-expression of circ-CUX1 led to altered expression of 1215 human mRNAs, including 781 up-regulated genes and 434 down-regulated genes. Furthermore, we validated the RNA-seq results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to circ-CUX1 over-expression in human tumor cells, and these findings will help us understand the pathogenesis of tumor progression.
2019-11-07 | GSE136135 | GEO
Project description:Long noncoding RNAs (lncRNAs), one type of endogenous RNA longer than 200 nucleotides, play emerging roles in tumorigenesis and aggressiveness. However, the functions and underlying mechanisms of lncRNAs in regulating neuroblastoma progression still remain elusive. We identify HNF4A antisense RNA 1 (HNF4A-AS1), a lncRNA derived from upstream region of hepatocyte nuclear factor 4 alpha (HNF4A), as a novel driver of neuroblastoma progression. To investigate the mechanisms underlying the oncogenic functions of HNF4A-AS1, we employed the Illumina HiSeq X Ten as a discovery platform to analyze the transcriptome profiling changes of human neuroblastoma SH-SY5Y cells in response to stable over-expression of HNF4A-AS1. The results showed that stable over-expression of HNF4A-AS1 led to altered expression of 4296 human mRNAs, including 2169 up-regulated genes and 2127 down-regulated genes. Furthermore, we validated the RNA-seq results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to HNF4A-AS1 over-expression in human tumor cells, and these findings will help us understand the pathogenesis of tumor progression.
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