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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE157626 | GEO | 2021/06/02

REPOSITORIES: GEO

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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.

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

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

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

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Long Noncoding RNA HNF1A-AS1 Regulates Proliferation and Migration in Esophageal Adenocarcinoma Cells

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