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Next Generation Sequencing Facilitates Quantitative Analysis of chromatin conformational interaction between MYC and PVT1 in MCF7

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of chromatin conformational interaction between MYC and PVT1 in MCF7

PROVIDER: PRJNA415772 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6216930_1.fastq.gz	Fastqsanger.gz
	SRR6216930_2.fastq.gz	Fastqsanger.gz
	SRR6216931_1.fastq.gz	Fastqsanger.gz
	SRR6216931_2.fastq.gz	Fastqsanger.gz
	SRR6216932_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Facilitates Quantitative Analysis of chromatin conformational interaction between MYC and PVT1 in MCF7

Project description:MYC-PVT1 interaction is cell line specific

2018-05-31 | GSE106153 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of chromatin conformational interaction between MYC and PVT1 in MDA-MB-231, MCF7, HCT116 cancer cell line

Project description:MYC-PVT1 interaction is cell line specific

2018-05-31 | GSE97588 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of allele specific transcription of PVT1 and MYC in mouse nueronal progenitor clonal cells

Project description:PVT1 and MYC transcription is inversely correlated

2018-05-31 | GSE106197 | 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

2018-05-31 | GSE97585 | GEO

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

Project description:Induced MYC expression by CRISPRi targeting PVT1 was validated by RNA-seq

2018-05-31 | GSE97587 | GEO

N6-methyladenosine Modification of lncRNA Pvt1 Governs Epidermal Stemness

Project description:Dynamic chemical modifications of RNA represent novel and fundamental mechanisms that regulate stemness and tissue homeostasis. Rejuvenation and wound repair of mammalian skin are sustained by epidermal progenitor cells, which are localized within the basal layer of the skin epidermis. N6-methyladenosine (m6A) is one of the most abundant modifications found in eukaryotic mRNA and lncRNA (long non-coding RNA). In this report, we survey changes of m6A RNA methylomes upon epidermal differentiation, and identify Pvt1, a lncRNA whose m6A modification is critically involved in sustaining stemness of epidermal progenitor cells. With genome-editing and a mouse genetics approach, we show that ablation of m6A methyltransferase or Pvt1 impairs the self-renewal and wound healing capability of skin. Mechanistically, methylation of Pvt1 transcripts enhances its interaction with MYC and stabilizes the MYC protein in epidermal progenitor cells. Our study presents a global view of epitranscriptomic dynamics that occur during epidermal differentiation and identifies the m6A modification of Pvt1 as a key signaling event involved in skin tissue homeostasis and wound repair.

2021-02-01 | GSE165912 | GEO

A renal cancer-associated, renal tubule-specific, HIF-binding enhancer of oncogenic MYC and PVT1 expression

Project description:Clear cell renal cell carcinoma is characterized by loss of function of the von Hippel-Lindau tumor suppressor gene (VHL) and unrestrained activation of hypoxia inducible transcription factors (HIF). Genetic and epigenetic determinants can impact on HIF pathways. A recent genome-wide association study identified single nucleotide polymorphisms (SNPs) in an intergenic region on chromosome 8 that modify the risk of developing renal cancer. The SNPs are located in a putative regulatory region between the oncogenes MYC and PVT1. Using capture C assay and genome editing we show that HIF-binding to this regulatory element is necessary to trans-activate MYC and PVT1 expression specifically in cells of renal tubular origins. Moreover, we demonstrate that the risk associated polymorphisms increase chromatin accessibility and activity as well as binding of HIF to the enhancer. These findings further strengthen the hypothesis that genetic variation at HIF-binding sites modulates the oncogenic transcriptional output of the VHL-HIF axis and provide a functional explanation for disease associated effects of SNPs in ccRCC.

2017-02-12 | GSE84444 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of PVT1 overexpressed MDA-MB-231 cells.

Project description:PVT1 can regulates glycolysis related genes expression.

2024-05-01 | GSE175736 | GEO

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 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

2018-05-31 | GSE97584 | GEO