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

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

PROVIDER: PRJNA885478 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21755927_1.fastq.gz	Fastqsanger.gz
	SRR21755927_2.fastq.gz	Fastqsanger.gz
	SRR21755928_1.fastq.gz	Fastqsanger.gz
	SRR21755928_2.fastq.gz	Fastqsanger.gz
	SRR21755929_1.fastq.gz	Fastqsanger.gz

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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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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.

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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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Project description:Primary Myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by hyperplastic megakaryopoiesis and myelofibrosis. Through a gene expression profile (GEP) study we recently highlighted the upregulationof miR-34a-5p in PMF versus healthy donor (HD) CD34+ hematopoietic progenitor cells (HPCs). To shed some light into the role of miR-34a-5p in PMF pathogenesis, here we unravelled the effects of the overexpression of miR-34a-5p in HPCs forcing its expression in HPCs. We showed that enforced expression of miR-34a-5p blocks proliferation and favours the megakaryocyte and monocyte/macrophage commitment of HPCs. Interestingly, we identified lymphoid enhancer-binding factor 1 (LEF1) and nuclear receptor subfamily 4, group A, member 2 (NR4A2) transcripts as miR-34a-5p-targets downregulated after miR-34a-5p overexpression in HPCs as well as in PMF compared with HD HPCs. Remarkably, the knockdown of NR4A2 in HPCs mimicked the antiproliferative effects of miR-34a-5p overexpression, while the silencing of LEF1 phenocopied the effects of miR-34a-5p overexpression in HPCs lineage choice, by stimulating the megakaryocyte and monocyte/macrophage commitment.

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