Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Superenhancer-driven lncRNA FASRL in hepatocellular carcinoma [RNA-seq]

ABSTRACT: Superenhancers drive abnormal gene expression in tumors and promote malignancy. However, the relationship between superenhancer-associated lncRNA and abnormal metabolism is unknown.

ORGANISM(S): Homo sapiens

PROVIDER: GSE206548 | GEO | 2023/01/12

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Superenhancer-driven lncRNA FASRL in hepatocellular carcinoma [ChIP-seq]

Project description:Superenhancers drive abnormal gene expression in tumors and promote malignancy. However, the relationship between superenhancer-associated lncRNA and abnormal metabolism is unknown.

2023-01-12 | GSE206547 | GEO

Superenhancer-driven lncRNA FASRL in hepatocellular carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-01-12 | GSE206549 | GEO

STAT5-mediated chromatin interactions in superenhancers activate IL-2 highly inducible genes: Functional dissection of the Il2ra gene locus

Project description:Cytokines critically control immune responses, but how regulatory programs are altered to allow T cells to differentially respond to distinct cytokine stimuli remains poorly understood. Here, we have globally analyzed enhancer elements bound by IL-2-activated STAT5 and IL-21-activated STAT3 in T cells and identified Il2ra as the top-ranked gene regulated by an IL-2-activated STAT5-bound superenhancer and one of the top genes regulated by STAT3-bound superenhancers. Moreover, we found that STAT5 binding was rapidly superenriched at genes highly induced by IL-2 and that IL-2-activated STAT5 binding induces new and augmented chromatin interactions within superenhancer-containing genes. Based on chromatin interaction analysis by paired-end tag (ChIA-PET) sequencing data, we used CRISPR-Cas9 gene editing to target three of the STAT5 binding sites within the Il2ra superenhancer in mice. Each mutation decreased STAT5 binding and altered IL-2-induced Il2ra gene expression, revealing that individual elements within the superenhancer were not functionally redundant and that all were required for normal gene expression. Thus, we demonstrate cooperative utilization of superenhancer elements to optimize gene expression and show that STAT5 mediates IL-2-induced chromatin looping at superenhancers to preferentially regulate highly inducible genes, thereby providing new insights into the mechanisms underlying cytokine-dependent superenhancer function.

2017-10-30 | GSE102317 | GEO

Superenhancer-activation of KLHDC8A Drives Glioma Ciliation and Hedgehog signaling

Project description:Glioblastoma ranks among the most aggressive and lethal of all human cancers, with poor responses to all therapeutic modalities. Self-renewing, highly tumorigenic glioblastoma stem cells (GSCs) contribute to therapeutic resistance and maintain cellular heterogeneity. Identification of GSC vulnerabilities may provide novel therapeutic targets for treating glioblastoma. Here, we interrogated superenhancer landscapes of primary glioblastoma specimens and patient-derived GSCs, revealing a kelch domain-containing gene (KLHDC8A) with a previously unknown function as an epigenetically driven oncogene. Targeting KLHDC8A decreased GSC proliferation, reduced sphere formation, induced apoptosis, and impaired in vivo tumor growth. Transcription factor control circuitry analyses revealed that the master transcriptional regulator SOX2 contributes to KLHDC8A expression. Mechanistically, KLHDC8A functions in the assembly of primary cilia via interactions with Chaperonin-containing TCP1 (CCT) and establishes a platform for a critical stem-specific signaling node through the Hedgehog pathway. Furthermore, we identified that Hedgehog and Aurora B/C Kinase signaling are complementary in GSCs, and dual inhibition synergistically inhibits GSC proliferation. Collectively, superenhancers enrich for essential mediators of cellular identity and offer a novel regulatory mechanism whereby promotion of ciliogenesis establishes and maintains a core GSC signaling node via the Hedgehog pathway, potentially offering insights into therapeutic vulnerabilities for glioblastoma treatment.

2022-12-22 | GSE207760 | GEO

HHIP-AS1 lncRNA promotes tumorigenicity in human SHH-driven brain tumors

Project description:Long non-coding RNAs (lncRNAs) comprise a diverse class of gene expression regulators with emerging roles in many biological processes including cancer. Here we show that the expression of the lncRNA Hedgehog Interacting Protein Antisense 1 (HHIP-AS1) is a hallmark feature of human SHH-driven tumors. Importantly, loss of HHIP-AS1 leads to reduced tumor growth in SHH-driven tumors in vitro and in vivo. Our results demonstrate the power of cross-entity transcriptome-wide comparisons to identify novel epigenetic–regulatory lncRNA circuitries underlying human cancers.

2022-06-01 | PXD016550 | Pride

Vector and Brown fat lncRNA 1 (Blnc1) expressing differentiated brown adipocytes

Project description:Blnc1 is a novel nuclear lncRNA that promotes brown and beige adipocyte differentiation and function. Blnc1 forms a ribonucleoprotein complex with transcription factor EBF2 to stimulate the thermogenic gene program. Further, Blnc1 itself is a target of EBF2, thereby forming a feedforward regulatory loop to drive adipogenesis toward thermogenic phenotype. We used microarrays to elucidate the role of Blnc1 on brown adipocyte differentiation and the induction of the thermogenic gene program. Brown adipocytes expressing vector or brown fat lncRNA 1 (blnc1) were differentiated for 6 days and harvested for RNA isolation and microarray using Affymetrix Mouse MG-430 PM Strip arrays. Two replicated samples were included in this study.

2015-02-28 | E-GEOD-55551 | biostudies-arrayexpress

ChIRP-MS of the lncRNA SAMMSON in uveal melanoma

Project description:Long non-coding RNAs (lncRNAs) can exhibit cell-type or even cancer-type specific expression profiles, making them highly attractive as therapeutic targets. PAN cancer RNA sequencing data revealed sustained expression of the SAMMSON lncRNA in uveal melanoma (UM), the most common primary intraocular malignancy in adults. Currently, there are no effective treatments for UM patients with metastatic disease, resulting in a median survival time of 6-12 months. We aimed to investigate the therapeutic potential of SAMMSON inhibition in UM.

2021-10-04 | PXD023511 | Pride

Scramble and Brown fat lncRNA 1 knockdown (shBlnc1) expressing differentiated brown adipocyte

Project description:Blnc1 is a novel nuclear lncRNA that promotes brown and beige adipocyte differentiation and function. Blnc1 forms a ribonucleoprotein complex with transcription factor EBF2 to stimulate the thermogenic gene program. Further, Blnc1 itself is a target of EBF2, thereby forming a feedforward regulatory loop to drive adipogenesis toward thermogenic phenotype. We used microarrays to elucidate the role of Blnc1 on brown adipocyte differentiation and mitochondrial function. Brown adipocytes expressing Scramble or brown fat lncRNA 1 knockdown (shBlnc1) were differentiated for 6 days and harvested for RNA isolation and microarray using Affymetrix Mouse MG-430 PM Strip arrays. Two replicated samples were included in this study.

2015-02-28 | E-GEOD-57540 | biostudies-arrayexpress

Expression profiling of lncRNA and mRNA in Hepatocellular carcinoma

Project description:To explore critical roles of lncRNA and mRNA playing in the pathogenesis of hepatocellular carcinoma, the Agilent microarray was used to simultaneously profile lncRNA and mRNA expression in 7 pairs of HCC and matched adjacent tumor-free tissues.

2019-08-06 | GSE101728 | GEO

Role of UPF1 in lncRNA-HEIH regulation for hepatocellular carcinoma therapy

Project description:To investigate UPF1 can regulates lncRNA-HEIH transcripts and function of lncRNA-HEIH, we established UPF1 knock out HeLa cell using CRISPR/cas9 system and overexpressed lncRNA-HEIH using plasmids.

2024-02-01 | GSE216667 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data