Bulk RNA Sequencing of XIST-knockdown A431 Cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA828573 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18839644.fastq.gz | Fastqsanger.gz | |||
| SRR18839645.fastq.gz | Fastqsanger.gz | |||
| SRR18839646.fastq.gz | Fastqsanger.gz | |||
| SRR18839647.fastq.gz | Fastqsanger.gz | |||
| SRR18839648.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 28 |
Similar Datasets
Project description:Systemic Lupus Erythematosus (SLE) is among the most sex-biased autoimmune diseases identified to date, affecting 9-times more women than men. Recognition of self-RNA by Toll-like receptor 7 (TLR7) is implicated as a central pathogenic process leading to the aberrant production of type-I interferon (IFN) in SLE, but the specific RNA molecules contributing to this process have not been defined. Given the role of self-RNA and biological sex in SLE pathogenesis, we investigated which sex-biased self-RNAs are potentially responsible for aberrant TLR7 activation in SLE. We used recent revelations about TLR7 sequence specificity and publicly available RNA sequencing data to identify sex-biased sources of self-RNA containing TLR7 ligands. We found X-inactive specific transcript (XIST) to be a particularly rich source of TLR7 ligands that is specifically expressed in women. We then investigated the capacity of XIST to act as a TLR7 ligand in vitro and found that multiple fragments of XIST induce IFNα production in a TLR7-dependent manner more than control RNA of equal length. Furthermore, we found that RNA isolated from XIST-knockout cells have significantly reduced capacity to stimulate TLR7 compared to RNA from wild-type cells. Finally, we used flow cytometry and publicly available RNA sequencing data to investigate the connection between XIST and SLE disease variables. We found that higher XIST expression correlated with SLE disease status, higher SLE disease activity index (SLEDAI) scores, and the interferon signature. Our data suggest that XIST is a source of TLR7 ligands that may underlie the sex bias in SLE.
2023-11-15 | GSE201160 | GEO
Project description:Cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer, and its incidence is increasing globally. In this study, Homeobox A9 (HOXA9), a direct target of onco-miR-365, was identified to be significantly down-regulated in CSCC tumors and cell lines. We conducted RNA sequencing to characterize gene expression changes in HOXA9-silenced cutaneous squamous cell carcinoma cells（A431）.
2018-03-12 | GSE100144 | GEO
Project description:Cutaneous squamous cell carcinoma (CSCC) is the most common metastatic skin cancer, and its incidence is increasing globally. In this study, metastasis-associated in lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA, was identified to be significantly up-regulated in CSCC tumors and cell lines. We conducted RNA sequencing to characterize gene expression changes in MALAT1-silenced cutaneous squamous cell carcinoma cells (A431).
2018-06-23 | GSE100399 | GEO
Project description:XIST is a long non-coding RNA (lncRNA) that mediates transcriptional silencing of X chromosome genes. Here we show that XIST is highly methylated with at least 78 N6-methyladenosine (m6A) residues, a reversible base modification whose function in lncRNAs is unknown. We show that m6A formation in XIST, as well as cellular mRNAs, is mediated by RBM15 and its paralog RBM15B, which bind the m6A-methylation complex and recruit it to specific sites in RNA. This results in methylation of adenosines in adjacent m6A consensus motifs. Furthermore, knockdown of RBM15 and RBM15B, or knockdown of the m6A methyltransferase METTL3 impairs XIST-mediated gene silencing. A systematic comparison of m6A-binding proteins shows that YTHDC1 preferentially recognizes m6A in XIST and is required for XIST function. Additionally, artificial tethering of YTHDC1 to XIST rescues XIST-mediated silencing upon loss of m6A. These data reveal a pathway of m6A formation and recognition required for XIST-mediated transcriptional repression. Three to four biological HEK293T replicates were used to perform iCLIP of endogenous YTH proteins, RBM15, and RBM15B. Crosslinking induced truncations were identified using CIMS-CITS pipeline.
2016-09-07 | E-GEOD-78030 | biostudies-arrayexpress
Project description:Transcriptional profiling of human epidermoid carcinoma cell comparing control A431-P cells with highly invasive subline A431-III cells
2013-06-18 | GSE47996 | GEO
Project description:Transcriptional profiling of human epidermoid carcinoma cell comparing control A431-P cells with highly invasive subline A431-III cells No treatmentt, A431-P cells vs. A431-III cells. A431-P cells are used as a reference to invstigate A431-III cells.
2013-06-18 | E-GEOD-47996 | biostudies-arrayexpress
Project description:XIST is a long non-coding RNA (lncRNA) that mediates transcriptional silencing of X chromosome genes. Here we show that XIST is highly methylated with at least 78 N6-methyladenosine (m6A) residues, a reversible base modification whose function in lncRNAs is unknown. We show that m6A formation in XIST, as well as cellular mRNAs, is mediated by RBM15 and its paralog RBM15B, which bind the m6A-methylation complex and recruit it to specific sites in RNA. This results in methylation of adenosines in adjacent m6A consensus motifs. Furthermore, knockdown of RBM15 and RBM15B, or knockdown of the m6A methyltransferase METTL3 impairs XIST-mediated gene silencing. A systematic comparison of m6A-binding proteins shows that YTHDC1 preferentially recognizes m6A in XIST and is required for XIST function. Additionally, artificial tethering of YTHDC1 to XIST rescues XIST-mediated silencing upon loss of m6A. These data reveal a pathway of m6A formation and recognition required for XIST-mediated transcriptional repression.
2016-09-07 | GSE78030 | GEO
Project description:Expression data to parental A431 VS CD109 KO A431
| PRJNA482298 | ENA
Project description:Autoimmune diseases disproportionately affect females more than males. The XX sex chromosome complement is strongly associated with susceptibility to autoimmunity. Xist long noncoding RNA (lncRNA) is expressed only in females to randomly inactivate one of the two X chromosomes to achieve gene dosage compensation. Here, we show that the Xist ribonucleoprotein (RNP) complex, comprised of numerous autoantigenic components, is an important driver of sex-biased autoimmunity. Inducible transgenic expression of a non-silencing form of Xist in male mice introduced Xist RNP complexes and sufficed to produce autoantibodies. Male SJL/J mice expressing transgenic Xist developed more severe multiorgan pathology in pristane-induced model of lupus than wild-type males. Xist expression in males reprogrammed T and B cell population and chromatin states to more resemble wild type females. Human patients with autoimmune diseases displayed significant autoantibodies to multiple components of XIST RNP. Thus, a sex-specific lncRNA scaffolds ubiquitous RNP components to drive sex-biased immunity.
2024-02-01 | GSE249828 | GEO
Project description:TCF4 was silenced in cutaneous squamous cell carcinoma of A431 cells, and detected the mRNA profiles compared to the negative control and blank control.
2019-07-06 | E-MTAB-7372 | biostudies-arrayexpress