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Transcriptome Analysis of Wild Type and FGD5-AS1 knockdown CCC-HEH-2 cells

ABSTRACT: Transcriptome Analysis of Wild Type and FGD5-AS1 knockdown CCC-HEH-2 cells

PROVIDER: PRJNA662264 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12607007_1.fastq.gz	Fastqsanger.gz
	SRR12607007_2.fastq.gz	Fastqsanger.gz
	SRR12607008_1.fastq.gz	Fastqsanger.gz
	SRR12607008_2.fastq.gz	Fastqsanger.gz
	SRR12607009_1.fastq.gz	Fastqsanger.gz

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Chromatin accessibility data in Wild Type and FGD5-AS1 knockdown CCC-HEH-2 cells (ATAC-Seq)

Project description:Purpose: According to the previous analysis results of gene regulation in fetal heart tissues with tetralogy of Fallot (ToF), we constructed the ceRNA mediated network driven by lncRNAs using a causal inference framework based on the expression correlations and validated miRNA-lncRNA/mRNA evidences. Totally 4 lncRNAs were identified as hub lncRNAs in the network, and FGD5-AS1 was focused for further loss-of-function investigation. Methods: The specific shRNAs against FGD5-AS1 (sh-FGD5-AS1) as well as the corresponding negative control (sh-NC) were constructed along with lentiviral vector respectively. Then the CCC-HEH-2 human cardiac myocytes cell lines were infected with lentivirus and followed puromycin treatment for several days. The knockdown efficiencies of the FGD5-AS1 expression were validated by qPCR. The landscape of accessible chromatin in control and knockdown CCC-HEH-2 cell lines were observed using ATAC-Seq. Conclusions: Our data reveal a unique different chromatin state between wild type and FGD5-AS1 knockdown CCC-HEH-2 cells.

2021-06-02 | GSE159464 | GEO

Transcriptome Analysis of Wild Type and FGD5-AS1 knockdown CCC-HEH-2 cells

Project description:Purpose: According to the previous analysis results of gene regulation in fetal heart tissues with tetralogy of Fallot (ToF), we constructed the ceRNA mediated network driven by lncRNAs using a causal inference framework based on the expression correlations and validated miRNA-lncRNA/mRNA evidences. Totally 4 lncRNAs were identified as hub lncRNAs in the network, and FGD5-AS1 was focused for further loss-of-function investigation. Methods: The specific shRNAs against FGD5-AS1 (sh-FGD5-AS1) as well as the corresponding negative control (sh-NC) were constructed along with lentiviral vector respectively. Then the CCC-HEH-2 human cardiac myocytes cell lines were infected with lentivirus and followed puromycin treatment for several days. The knockdown efficiencies of the FGD5-AS1 expression were validated by qPCR. Genome-wide RNA expression of control and knockdown CCC-HEH-2 cell lines were observed using RNA-Seq. Conclusions: Knockdown of this lncRNA interferes with glutamate receptor activity and metalloendopeptidase inhibitor activity. The expression of abundant CHD genes with |fold change| ≥ 2 was validated with qPCR. These results indicate that FGD5-AS1 plays an important role in CHD genes regulation networks.

2021-06-02 | GSE157626 | GEO

Chromatin accessibility data in Wild Type and FGD5-AS1 knockdown CCC-HEH-2 cells (ATAC-Seq)

Project description:Chromatin accessibility data in Wild Type and FGD5-AS1 knockdown CCC-HEH-2 cells (ATAC-Seq)

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Identification of downstream target genes of transcription factor ZEB1, lncRNA FGD5-AS1 and miR-34a-5p in gastric cancer

Project description:As one of the most abundant lncRNAs in cells, the biological function of lncRNA FGD5-AS1 remains largely unclear in cancers, especially in gastric cancer (GC). In addition, the reason for such high levels of FGD5-AS1 in cells remains unknown. In this study, FGD5-AS1 was proved to be a ZEB1-related lncRNA which was overexpressed and predicted poor prognosis in GC. Knockdown of FGD5-AS1 decreased GC proliferation in vitro and in vivo.

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Project description:ASYMMETRIC LEAVES 1 (AS1) is an important transcription factor for leaf development in Arabidopsis. But how it regulates downstream genes is largely unknown. We found a co-factor of AS1, LIKE HETEROCHROMATIN PROTEIN 1 (LHP1), also named as TERMINAL FLOWER 2 (TFL2), a PcG protein in Arabidopsis. To further investigate how AS1 and LHP1 co-regulate downstream genes at the genome level, we perform the transcriptome analysis of as1-1, tfl2-1, and as1-1 tfl2-1 in comparison with wild type (WT).

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Analysis of genes regulated by AS1 and AS2

Project description:AS1 and AS2 encode MYB related protein and AS2-domain containing protein, respectively and may regulate transcription. These genes are involved in the determination of axes of leaves of Arabidopsis thaliana. To know the gene regulation in the leaf development, expression profile among wild-type, as1 and as2 mutants and AS2 overexpression plants were compaired. shoot apices from as1-1, as2-1, AS2 overexpressing, and wild type embryos

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Project description:In this study, we used miRNA sequencing to analyze and identify possible miRNAs that can be regulated by and ELF3-AS1 in gastric cancer. The results showed that lncRNA ELF3-AS1 knockdown decreased the expression of miR-33a/b and miR-203a. Due to miR-33a/b and miR-203a were able to target SNAI2 expression, and ELF3-AS1 knockdown significantly upregulates SNAI2 expression, we speculated ELF3-AS1 may negatively regulate SNAI2 expression through positively regulating the expression of miR-33a/b and miR-203a in GC.

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Gene expression microarray analysis of NCK1-AS1 knockdown in CaSki cells

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2018-01-01 | GSE107171 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of SiHa cells with or without circCDKN2B-AS1 knockdown

Project description:circCDKN2B-AS1 is significantly upregulated circRNA in HPV16 positive cervical cancer tissues comprared with both HPV16 positive and HPV16 negative normal cervical tissues.So we chose it for further study.To explore the mRNA expression profiles following circCDKN2B-AS1 knockdown, we performed RNA sequencing analysis in SiHa cells with or without circCDKN2B-AS1 knockdown.We performed RNA sequencing in two pairs of RNA samples of SiHa cells with or without circCDKN2B-AS1 knockdown.

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Expression data from SKOV3.ip cells by knockdown RAD51-AS1 expression.

Project description:Long non-coding RNAs (lncRNA) have been shown to play crucial roles in tumorigenesis. Little is known about lncRNA RAD51-AS1 in diseases. Here, we investigated the role of RAD51-AS1 in Epithelial ovarian cancer. Silencing RAD51-AS1 inhibited proliferation through cell cycle arrest and promotion in apoptosis, both in vitro and in vivo. But the mechanism of RAD51-AS1 downstream regulation remains unclear. In order to identify the downstream regulation of RAD51-AS1 in epithelial ovarian cancer, we used antisene oligotides targeting RAD51-AS1 / negative control to transfect Skov3.ip cells. Then, we used microarrays to identified differential expression genes and to look for possible target genes by knockdown RAD51-AS1 expression.

2017-08-17 | GSE89374 | GEO

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