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Transcriptomic analysis of neuroblastoma cells in response to stable over-expression of circular RNA derived from CUX1 exons (ecircCUX1)

ABSTRACT: 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 public datasets, we identified circular RNA derived from CUX1 exons (ecircCUX1) as a novel driver of NB progression. To investigate the mechanisms underlying the oncogenic functions of ecircCUX1, we employed the BGIseq500 as a discovery platform to analyze the transcriptome profiling changes of human SH-SY5Y cells in response to stable over-expression of ecircCUX1. The results showed that stable over-expression of ecircCUX1 led to altered expression of 2155 human mRNAs, including 460 up-regulated and 1695 down-regulated genes. Then, we found the possible roles of these differentially regulated mRNAs in selected pathways including lipid metabolic reprogramming, mitochondrial complex I activity, 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 ecircCUX1 over-expression in human NB cells, and these findings will help us understand the pathogenesis of NB.

ORGANISM(S): Homo sapiens

PROVIDER: GSE182329 | GEO | 2021/10/06

REPOSITORIES: GEO

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Transcriptomic analysis of neuroblastoma cells in response to stable over-expression of circular RNA derived from CUX1 gene (circ-CUX1)

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

Transcriptomic analysis of neuroblastoma cells in response to stable over-expression of circular RNA derived from CUX1 gene (circ-CUX1)

Project description:Transcriptomic analysis of neuroblastoma cells in response to stable over-expression of circular RNA derived from CUX1 gene (circ-CUX1)

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Genomic studies controvert the existence of the CUX1 p75 isoform

Project description:CUX1, a homeodomain-containing transcription factor, is recurrently deleted or mutated in multiple tumor types. In myeloid neoplasms, CUX1 deletion or mutation carries a poor prognosis. We have previously established that CUX1 functions as a tumor suppressor in hematopoietic cells across multiple organisms. Others, however, have described oncogenic functions of CUX1 in solid tumors, often attributed to truncated CUX1 isoforms, p75 and p110. Given the clinical relevance, it is imperative to clarify these discrepant activities. Herein, we sought to determine the CUX1 isoforms expressed in hematopoietic cells, and find that they express the full-length p200 isoform. Through the course of this analysis, we found no evidence of the p75 alternative transcript in any cell type examined. Using an array of orthogonal approaches, including biochemistry, proteomics, CRISPR/Cas9 genomic editing, and analysis of functional genomics datasets across a spectrum of normal and malignant tissue types, we found no data to support the existence of the CUX1 p75 isoform generated by an alternative transcriptional start site. Based on these results, prior studies of p75 require reevaluation, including the interpretation of oncogenic roles attributed to CUX1.

2022-02-17 | PXD027527 | Pride

Functional genomic analysis of the haploinsufficient tumor suppressor, CUX1

Project description:CUX1 is a homeodomain-containing transcription factor that is conserved, ubiquitous, and essential in vertebrates and invertebrates. CUX1 is mutated or deleted in high-risk myeloid neoplasms and solid tumors, resulting in haploinsufficiency and tumor growth. Here we provide the first analysis of endogenous, whole genome, CUX1 DNA binding. We demonstrate that CUX1 binds with transcriptional activators and cohesin at distal enhancers across three different human cell types. Haploinsufficiency of CUX1 altered the expression of a large number of genes, including cell cycle regulators, with concomitant increased cellular proliferation. Surprisingly, CUX1 occupancy decreased genome-wide in the haploinsufficient state, and binding site affinity did not correlate with differential gene expression. Instead, differentially expressed genes had multiple, low-affinity CUX1 binding sites, consistent with an analog model for CUX1 gene regulation. A machine-learning algorithm determined that chromatin accessibility, enhancer activity, and distance to the transcription start site are features of functional CUX1 DNA binding. Moreover, CUX1 is enriched at sites of DNA looping, and these loops connect CUX1 to the promoters of target genes. We propose that CUX1 is an analog transcription factor that regulates target genes through higher order genome architecture.

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Transcriptomic analysis of neuroblastoma cells in response to stable over-expression of circular RNA derived from CUX1 exons (ecircCUX1)

Project description:Transcriptomic analysis of neuroblastoma cells in response to stable over-expression of circular RNA derived from CUX1 exons (ecircCUX1)

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Next generation sequencing following CUX1 knockdown in erythroblasts

Project description:Anemia is a significant cause of morbidity and mortality in myeloid malignances. Cytogenetic changes are recurrent within malignant hematopoietic stem and progenitor cells, yet their role in anemia pathogenesis remains unknown. One recurrent karyotypic abnormality in myeloid neoplasms is the deletion of part or all of chromosome 7 [-7/del(7q)], which harbors the transcription factor and tumor suppressor gene, CUX1. CUX1 knockdown mouse models develop myeloid disease similar to that seen in humans, including a spontaneous, cell intrinsic, and lethal anemia that develops with age. Here, we elucidate the cellular and molecular mechanisms by which CUX1 regulates erythropoiesis. We demonstrate CUX1 knockdown mice have an aberrant stress erythropoiesis response and decreased survival after acute anemia induction. CUX1 insufficient erythroblasts undergo accelerated cell cycling and increased apoptosis. In line with these phenotypes, transcriptome profiling indicates that CUX1-knockdown elicits increased proliferation and decreased erythroid differentiation gene signatures. ATAC-sequencing demonstrated dramatic, global chromatin opening in CUX1-knockdown erythroblasts. As measured by fluorescence lifetime imaging, this increased chromatin accessibility is concomitant with a disruption in nuclear condensation, which is normally requisite in mammalian erythroblasts for nuclear eviction and terminal differentiation. Finally, we show that CUX1 mediates chromatin compaction by promoting histone deacetylation. Thus, rather than a transcriptional role, our data implicate in an epigenetic regulatory role for CUX1 in erythropoiesis. Furthermore, these results suggest therapeutic targeting of epigenetic regulators, such as histone acetyl transferases, may have clinical benefit for the anemias associated with loss of CUX1.

2021-08-10 | GSE181626 | GEO

Transcriptomic analysis of neuroblastoma cells in response to stable over-expression of myeloid zinc finger 1 antisense RNA 1 (MZF1-AS1)

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 public datasets, we identified myeloid zinc finger 1 antisense RNA 1 (MZF1-AS1) as a novel lncRNA associated with the progression of NB. To investigate the mechanisms underlying the oncogenic functions of MZF1-AS1, 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 MZF1-AS1. The results showed that stable over-expression of MZF1-AS1 led to altered expression of 2920 human mRNAs, including 1476 up-regulated genes and 1444 down-regulated genes. Then we found the possible roles of these differentially regulated mRNAs in selected pathways including proline synthesis, 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 MZF1-AS1 over-expression in human NB cells, and these findings will help us understand the pathogenesis of NB.

2020-06-30 | GSE133009 | GEO

Transcriptomic analysis of neuroblastoma cells in response to stable over-expression of small peptide encoded by hepatocyte nuclear factor 4 alpha antisense RNA 1 (HNF4A-AS1)

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. We identified a small 51-amino acid peptide (sPEP1) encoded by hepatocyte nuclear factor 4 alpha antisense RNA 1 (HNF4A-AS1) in NB cells treated by serum deprivation. To investigate the mechanisms underlying the oncogenic functions of sPEP1, 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 sPEP1. The results showed that stable over-expression of sPEP1 led to altered expression of 2543 human mRNAs, including 2457 up-regulated genes and 86 down-regulated genes. Then we found the possible roles of these differentially regulated mRNAs in selected pathways including stemness, senescence, 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 sPEP1 over-expression in human NB cells, and these findings will help us understand the pathogenesis of NB.

2023-05-15 | GSE193815 | GEO

Transcriptomic analysis of neuroblastoma SH-SY5Y cells in response to stable over-expression of neuroblastoma highly expressed 1 (NHEG1)

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: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.

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