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Validation of AS1 as novel regulator of tumor resistance to immune cell attack

ABSTRACT: Validation of AS1 as novel regulator of tumor resistance to immune cell attack

PROVIDER: PRJNA408285 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6057320_1.fastq.gz	Fastqsanger.gz
	SRR6057320_2.fastq.gz	Fastqsanger.gz
	SRR6057311_1.fastq.gz	Fastqsanger.gz
	SRR6057311_2.fastq.gz	Fastqsanger.gz
	SRR6057321_1.fastq.gz	Fastqsanger.gz

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Validation of AS1 as novel regulator of tumor resistance to immune cell attack

Project description:The experiment was performed to verify wether knockdown of AS1 in combination with TNFa treatment affected the signature of genes involved in tumor cell apoptosis and survival

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

Project description:Objectives: Long non-coding RNAs (lncRNAs) have been shown to play important roles in the development and progression of cancer. However, functional lncRNAs and their downstream mechanisms are largely unknown in the molecular pathogenesis of esophageal adenocarcinoma (EAC) and its progression. Design: lncRNAs that are abnormally upregulated in EACs were identified by RNA-seq analysis, followed by quantitative RT-PCR (qRTPCR) validation using tissues from 31 EAC patients. Cell biological assays in combination with siRNA-mediated knockdown were performed in order to probe the functional relevance of these lncRNAs. Results: We discovered that a lncRNA, HNF1A-AS1, is markedly upregulated in human primary EACs relative to their corresponding normal esophageal tissues (mean fold change 7.2, p<0.01). We further discovered that HNF1A-AS1 knockdown significantly inhibited cell proliferation and anchorage independent growth, suppressed S-phase entry, and inhibited cell migration and invasion in multiple in vitro EAC models (p<0.05). A gene ontological analysis revealed that HNF1A-AS1 knockdown preferentially affected genes that are linked to assembly of chromatin and the nucleosome, a mechanism essential to cell cycle progression. The well-known cancer-related lncRNA, H19, was the gene most markedly inhibited by HNF1A-AS1 knockdown. Consistent to this finding, there was a significant positive correlation between HNF1A-AS1 and H19 expression in primary EACs (p<0.01). In order to identify novel oncogenic lncRNAs in esophageal adenocarcinogenesis, we carried out RNA-seq of a matched NE-BE-EAC tissue pair

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Effects of SOCS2-AS1 inhibition in prostate cancer cells

Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. We identified a novel androgen-regulated long non-coding (lnc) RNA, SOCS2-AS1. In order to investigate the SOCS2-AS1 function in prostate cancer cells, we performed gene expression in AR-positive prostate cancer cell lines (LNCaP and LTAD) after siSOCS2-AS1 or siSOCS2 treatment. We also treated cells with vehicle or androgen to analyzed the effects of siSOCS2-AS1 on AR function. Observation of androgen dependent gene expression changes after treatmet with siSOCS2-AS1 with microarray.

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Analysis of direct target genes regulated by AS1 and AS2

Project description:Analysis of tiling array data identified 358 genomic regions commonly enriched by the AS1 and T7 antibody datasets. AS1 antibody data set (AS1 antibody versus mock) and the T7 antibody data set (T7 antibody versus mock)

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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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Identification of LncRNA TRAF3IP2-AS1 as a key regulator of IL-17 signaling through the SRSF10-IRF1-Act1 axis in autoimmune diseases

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short and long attack latency mice

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