Transcriptomic analysis of neuroblastoma cells in response to stable over-expression of armadillo repeat containing 12 (ARMC12)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA420394 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6331508_1.fastq.gz | Fastqsanger.gz | |||
| SRR6331508_2.fastq.gz | Fastqsanger.gz | |||
| SRR6331509_1.fastq.gz | Fastqsanger.gz | |||
| SRR6331509_2.fastq.gz | Fastqsanger.gz |
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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:Recent studies suggest the emerging roles of armadillo (ARM) family proteins in tumor progression. However, the functions and underlying mechanisms of ARM members in tumorigenesis and aggressiveness of neuroblastoma (NB) remain to be determined. Herein, we identify armadillo repeat containing 12 (ARMC12) as an ARM member associated with NB progression. ARMC12 promotes the growth and aggressiveness of NB cell lines. Mechanistically, ARMC12 physically interacts with retinoblastoma binding protein 4 (RBBP4) to facilitate the formation and activity of polycomb repressive complex 2, resulting in transcriptional repression of tumor suppressive genes. Blocking the interaction between ARMC12 and RBBP4 by cell-penetrating inhibitory peptide activates the downstream gene expression and suppresses the tumorigenesis and aggressiveness of NB cells. Both ARMC12 and RBBP4 are upregulated in NB tissues, and are associated with unfavorable outcome of patients. These findings suggest the crucial roles of ARMC12 in tumor progression and a potential therapeutic approach for NB.
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Project description:Longitudinal study of armadillo transcription.
2023-10-10 | GSE141951 | 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.
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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.
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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 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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