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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptome profile of silenced MCF-7 using ASO mediated knock-down for three lncRNAs

ABSTRACT: RNA-Seq of MCF-7 knock-down cells for PVT1, FGD5-AS1, and EPB41L4A-AS1. Cells were treated with ASO or scramble as negative control.

INSTRUMENT(S): Illumina NovaSeq 6000, none, DELL PRICISION T7500

ORGANISM(S): Homo sapiens

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PROVIDER: E-MTAB-14148 | biostudies-arrayexpress |

SECONDARY ACCESSION(S): E-MTAB-14147

REPOSITORIES: biostudies-arrayexpress

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Nascent transcriptome profile of silenced MCF-7 using ASO mediated knock-down for PVT1

Project description:Nascent-Seq of MCF-7 knock-down cells for PVT1. Cells were treated with ASO or scramble as negative control.

2025-02-14 | E-MTAB-14149 | biostudies-arrayexpress

Nuclear RNA immunoprecipitation of ERα in MCF-7 BC cell line

Project description:Native nuclear RNA immunoprecipiatation of the estrogen receptor α (ERα) in exponentially growing MCF-7 for the identification of RNAs linked to the receptor.

2025-02-14 | E-MTAB-14147 | biostudies-arrayexpress

Human uterine Natural Killer cells regulate differentiation of extravillous trophoblast early in pregnancy - bulk RNA-seq data

Project description:An allorecognition system depending on interactions between uterine Natural Killer (uNK) cells and placental extravillous trophoblast (EVT) during early pregnancy influences reproductive outcomes in humans. Our previous immunogenetic studies show that particular combinations of maternal Killer Immunoglobulin-like Receptors (KIR) in uNK cells with fetal HLA-C variants on EVT are associated with disorders of pregnancy, especially pre-eclampsia. To identify responses stimulated in uNK cells specifically when activating KIR (KIR2DS1) binds to C2+HLA-C, a combination protective against pre-eclampsia, we modelled KIR-HLA interactions by co-culturing uNK cells with the 721.221 HLA-null cell line transfected to express either C1+ or C2+HLA-C molecules, followed by transcriptome profiling by RNA sequencing. We detect the secretion of key cytokines by uNK cells under the protective combination between KIR2DS1 and C2+HLA-C.

2024-01-10 | E-MTAB-13379 | biostudies-arrayexpress

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Long non-coding RNA PVT1 is overexpressed in cutaneous squamous cell carcinoma and exon 2 is critical for its oncogenicity

Project description:Background Cutaneous squamous cell carcinoma (cSCC) is one of the most common and fastest increasing forms of cancer worldwide with metastatic potential. Long non-coding RNAs (lncRNAs) are a group of RNA-molecules with essential regulatory functions for both physiological and pathological processes. Objectives To investigate the function and mode of action of lncRNA plasmacytoma variant translocation 1 (PVT1) in cSCC. Methods The expression level of PVT1 was quantified in healthy skin, benign skin diseases and cSCCs by qRT-PCR and single molecule in situ hybridization. The function of PVT1 in cSCC was investigated both in vivo (tumour xenograft) and in vitro (competitive cell growth assay, EdU-incorporation assay, colony formation assay and tumour spheroid formation assay) by CRISPR-Cas9-mediated PVT1 or PVT1 exon 2 knockout and by locked nucleic acid (LNA) GapmeR-mediated PVT1-knockdown. RNAseq-analysis was conducted to identify genes and processes regulated by PVT1. Results We identified PVT1 as a lncRNA upregulated in cutaneous squamous cell carcinoma in situ (cSCCIS) and cSCC and associated with oncogenic phenotype of cSCC. The increased expression of PVT1 in cSCC was regulated by MYC. Both CRISPR-Cas9-deletion of the entire PVT1 locus and LNA GapmeR-mediated knockdown of PVT1-transcript impaired malignant behaviour of cSCC cells which suggested that PVT1 is an oncogenic transcript in cSCC. Furthermore, knockout of PVT1 exon 2 inhibited cSCC tumour growth both in vivo and in vitro demonstrating that exon 2 is a critical element for the oncogenic role of PVT1. Mechanistically, we show that PVT1 is localized in the cell nucleus and acts as a suppressor of cellular senescence by inhibiting CDKN1A expression and preventing cell cycle arrest. Conclusions Our study reveals a previously unrecognized role for exon 2 of PVT1 in its oncogenic role and that PVT1 suppresses cellular senescence. PVT1 may be a biomarker and therapeutic target in cSCC.

2023-11-30 | GSE235606 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis for H3K27ac mediated chromatin conformation capture of Wild Type and PVT1 Knockdown by CRISPRi in MDA-MB-231 human breast cancer cell line

Project description:CRISPRi targeting PVT1 specifically decrease PVT1-MYC interaction

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Next Generation Sequencing Facilitates Quantitative Analysis for Chromatin Immunoprecipitation of Wild Type and PVT1 Knockdown by CRISPRi in MDA-MB-231 human breast cancer cell line

Project description:CRISPRi targeting PVT1 specifically increased H3K9me3 at PVT1

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2024-09-18 | E-MTAB-13565 | biostudies-arrayexpress

TTF1 control of LncRNA synthesis and cell growth delineates a tumour suppressor pathway acting directly on the ribosomal RNA Genes

Project description:The tumour suppressor p14/19ARF regulates ribosomal RNA (rRNA) synthesis by controlling the nucleolar localization of Transcription Termination Factor 1 (TTF1). However, the role played by TTF1 in regulating the rRNA genes and in potentially controlling growth has remained unclear. We now show that TTF1 expression regulates cell growth by determining the cellular complement of ribosomes. Unexpectedly, it achieves this by acting as a “roadblock” to synthesis of the non-coding LncRNA and pRNA that we show are generated from the “Spacer Promoter” duplications present upstream of the 47S pre-rRNA promoter on the mouse and human ribosomal RNA genes. Unexpectedly, the endogenous generation of these non-coding RNAs does not induce CpG methylation or gene silencing. Rather, it acts in cis to suppress 47S preinitiation complex formation and hence de novo pre-rRNA synthesis by a mechanism reminiscent of promoter interference or occlusion. Taken together, our data delineate a pathway from p19ARF to cell growth suppression via the regulation of ribosome biogenesis by non-coding RNAs and validate a key cellular growth law in mammalian cells.

2024-12-31 | E-MTAB-13820 | biostudies-arrayexpress

Transcriptomic analysis by AmpliSeq Ion Torrent to explore the effects of the long non-coding RNA TGFB2-AS1 on gene expression in human keratinocytes

Project description:TGFB2-AS1 is a long non-coding RNA which is induced by ΤGFβ signaling. In order to assess the importance of TGFB2-AS1 on the regulation of gene expression, we performed an AmpliSeq transcriptomic array in human keratinocytes (HaCaT), which stably over-express TGFB2-AS1 or control pcDNA3 empty vector. In addition, cells were stimulated with TGFβ1 for 24 hours, in order to observe the effects of TGFB2-AS1 on gene expression, downstream of TGFβ signaling. RNA from the following four conditions was used in this experiment: 1) pcDNA3, 2) pcDNA3+TGFβ1, 3) pcDNA3-TGFB2-AS1, 4) pcDNA3-TGFB2-AS1+TGFβ1. Biological triplicates were used per condition.

2019-07-01 | E-MTAB-7773 | biostudies-arrayexpress

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