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)
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ABSTRACT:
PROVIDER: PRJNA798034 | ENA |
REPOSITORIES: ENA
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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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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.
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Project description:NFYC-AS1 is an overlapping antisense RNA transcribed head-to-head to NFYC sense gene, encoding for the subunit C of NF-Y transcription factor, which is known as master regulator of cell cycle and proliferation in normal and tumor cells. Here we performed NFYC-AS1 silencing in lung squamous carcinoma H520 cells by Gapmer antisense oligonucleotides and CRISPR/Cas9 TSS deletion. Afterwards, we performed differentially expressed analysis and gene set enrichement analysis to investigate on NFYC-AS1 function and mechanism of action.
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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.
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Project description:LncRNA Hypoxia-inducible factor 1α-antisense 1 (HIF1α-AS1) is located on the antisense strand of the important Hypoxia-inducible factor 1α (HIF1α) gene, but being transcribed in antisense direction along the HIF1α promoter. Here we used the 3’end biotinylated HIF1a-AS1 RNA and a control RNA for RNA Pulldown and searched for interacting proteins in nuclear extracts of human umbilical vein endothelial cells (HUVEC).
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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 publically available microarray datasets, we discovered a novel 963-bp lncRNA, named FOXD3 antisense RNA 1 (FOXD3-AS1), as an independent prognostic marker for favorable clinical outcome of NB patients. To investigate the mechanisms underlying the oncogenic functions of FOXD3-AS1, we employed the Illumina HiSeq PE125/PE150 as a discovery platform to analyze the transcriptome profiling changes of human BE(2)-C cells in response to stable over-expression of FOXD3-AS1. The results showed that stable over-expression of FOXD3-AS1 led to altered expression of 3191 human mRNAs, including 1542 up-regulated genes and 1650 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 RNA-seq results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to FOXD3-AS1 over-expression in human NB cells, and these findings will help us understand the pathogenesis of NB.
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Project description:Long non-coding RNA NR2F1 antisense RNA1 (lncRNA NR2F1-AS1) was identified as the main candidate associated to late recurrence in ER-positive breast cancer clinical samples. Gain-of-function of NR2F1-AS1 induced the expression of dormancy-inducers BMP4 and DEC2, and upregulated pluripotency markers NANOG and OCT4. Representative pathways entailed to metastatic events such as HER2/Neu, hypoxia, EMT and inflammatory-response were also found enriched.
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Project description:Monocytes are key players in innate immunity, with their ability to regulate inflammatory responses and combat invading pathogens. There is a growing body of evidence indicating that long non-coding RNA (lncRNA) participate in various cellular biological processes, including the innate immune response. The immunoregulatory properties of numerous lncRNAs discovered in monocytes remain largely unexplored. In this study, we used RNA sequencing data of circulatory blood monocytes obtained from sepsis patients to identify the elevated antisense lncRNA JHMD1D-AS1, relative to healthy participants. We subsequently demonstrated that in both circulatory blood monocytes and monocyte-derived macrophages exposed to TLR-agonists, JHMD1D-AS1 expression was induced in a temporal specific manner. Using small interfering RNA (siRNA) electroporation to render monocytes deficient of JHDM1D-AS1 and over-expression experiments, we revealed a role for lncRNA JHDM1D-AS1 in cell development, as well as in restraining pro-inflammatory gene expression. Altogether, these findings identify antisense lncRNA JHDM1D-AS1 as a potential repressor of the inflammatory response in human primary monocytes and macrophages.
2022-05-07 | GSE201958 | 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 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.
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