Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

AEBP1-GLI1 pathway attenuates the FACT complex dependency of bladder cancer cell survival.

ABSTRACT: AEBP1 expression predicts a poor prognosis of bladder cancer patients, while its role has not been fully understood. We here show that the expression of AEBP1 was correlated with GLI transcriptional factors, leading to limit the SSRP1/SUPT16H (FACT) complex-dependency of bladder cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE288105 | GEO | 2025/06/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

AEBP1-GLI1 pathway attenuates the FACT complex dependency of bladder cancer cell survival.

Project description:AEBP1-GLI1 pathway attenuates the FACT complex dependency of bladder cancer cell survival.

| PRJNA1216201 | ENA

Silencing of AEBP1 in U87MG glial cells and Chip-chIP with AEBP1 antibody

Project description:AEBP1 has been identified as a transcriptional repressor playing a significant role in adipogenesis. Recently, we have found that AEBP1 is specifically upregulated in primary glioblastoma. We have used gene silencing to identify genes perturbed upon AEBP1 downregulation and ChIP-chip technique to identify its genomic targets of binding and regulation to understand the un-annotated/undescribed role of this transcription factor in gliomagenesis. Cells either mock silenced or silenced using siRNA against AEBP1 were harvested at 46hrs post transfection. Gene expression was profiled for control and AEBP1 silenced cells. comparison of AEBP1/Rabbit IgG/ Glial cells

2012-04-29 | E-GEOD-18892 | biostudies-arrayexpress

Silencing of AEBP1 in U87MG glial cells and Chip-chIP with AEBP1 antibody

2012-04-30 | GSE18892 | GEO

Effects of AEBP1 knockdown on gene expression profiles in HUVEC

Project description:We identified adipocyte enhancer binding protein 1 (AEBP1) as a novel tumor endothelial marker in colorectal cancer (CRC). To identify target genes of AEBP1 in endothelial cells, we knocked down AEBP1 in human umbilical vein endothelial cells (HUVECs). We found that genes associated with angiogenesis including aquaporin 1 (AQP1) and periostin (POSTN) are downregulated by AEBP1 knockdown in HUVECs, suggesting that AEBP1 may promote tumor angiogenesis through regulating these genes.

2020-04-01 | GSE138427 | GEO

Role of AEBP1 in LX-2 cells

Project description:To investigate the role of AEBP1 involved in hepatic stellate cells (HSCs), we inhibited AEBP1 expression by specific siRNA in human HSC line LX-2 cells. Total RNA was loaded for bulk RNA sequencing.

2023-10-19 | GSE219170 | GEO

Effects of AEBP1 knockdown on gene expression profiles in cancer-associated fibroblasts

Project description:We identified adipocyte enhancer binding protein 1 (AEBP1) as a novel cancer-associated fibroblast (CAF) marker in oral squamous cell carcinoma (OSCC). To study the function of AEBP1 in CAFs, we knocked down AEBP1 in CAFs isolated from surgically resected primary OSCCs. We found that genes associated with cell cycle were significantly affected by AEBP1 knockdown in CAFs.

2023-09-13 | GSE234220 | GEO

Effects of AEBP1 knockdown on gene expression profiles in human skeletal muscle myoblasts

Project description:We recently identified adipocyte enhancer binding protein 1 (AEBP1) as a novel cancer stroma-associated gene and reported that AEBP1 activates cancer-associated fibroblasts in oral cancer. In this study, we show that AEBP1 is negatively associated with skeletal muscle cell differentiation. We found that AEBP1 is downregulated during the diffraction of human skeletal muscle myoblasts (HSMMs). Microarray analysis revealed that knockdown of AEBP1 significantly upregulated a number of genes associated with myogenesis in HSMMs. Notably, co-culture of HSMMs with oral squamous cell carcinoma cells resulted in downregulation of muscle-related genes and upregulation of AEBP1 in HSMMs.

2024-11-14 | GSE268740 | GEO

Comparative chromatin accessibility profiling of wildtype and supt16h-/- zebrafish using ATAC-sequencing

Project description:Chromatin organization and accessibility are fundamental to how genes are transcriptionally controlled. We identify the first vertebrate mutant for supt16h, a component of the FACT (FAcilitates Chromatin Transcription) complex along with Ssrp1 known to reorganize nucleosomes and assist in transcriptional elongation. We demonstrate its importance in hematopoietic stem cell (HSC) specification by regulating the elongation of Notch genes. Unexpectedly, Assay for Transposase Accessible Chromatin (ATAC) sequencing revealed that loss of supt16h does not affect histone accessibility on a Notch-specific or global level. Although the majority of genes are unaffected, loss of supt16h alters chromatin accessibility significantly at the p53 locus, leading to its overexpression in mutants. Upon downregulation of p53, both loss of Notch and loss of HSC phenotypes are rescued. Notably, ssrp1 mutants possessed normal elongation of Notch genes, levels of P53, and specification of HSCs. Our results highlight the discrete effects of Supt16h and Ssrp1 during HSC specification. Additionally, we demonstrate the relationship between supt16h and p53 during transcriptional elongation to specify HSC fate via modulation of Notch signaling.

2020-09-01 | GSE106341 | GEO

RNA-sequencing based linkage analysis identifies supt16h as a target gene from a forward genetic screen

2020-09-01 | GSE106342 | GEO

Targeting of glioma stem-like cells with a parthenolide derivative ACT001 through inhibition of AEBP1/PI3K/AKT signaling

Project description:Glioblastoma (GBM) is the most lethal primary brain tumor in adults with a median survival of around 15 months. A potential treatment strategy involves targeting glioma stem-like cells (GSCs) that are able to initiate, maintain, and repopulate the tumor mass. Here, we identify ACT001, a parthenolide derivative, targeting GSCs through regulation of adipocyte enhancer binding protein 1 (AEBP1) signaling.GSCs exhibit high response to ACT001 in compared with normal human astrocytes. AEBP1 is a putative target of ACT001 by RNA-Seq analysis, which expression associates with prognosis of GBM patients. Knockdown of AEBP1 inhibits GSC proliferation whereas ectopic expression of AEBP1 increases GSC proliferation and xenograft tumor growth. AEBP1 overexpression also attenuates ATC001-inhibited GSC orthotopic xenograft tumor growth. Treatment with ACT001 or PI3K inhibitor or AEBP1 depletion decreases AKT phosphorylation and GSC proliferation. However, constitutive AKT activation rescues ACT001 treatment or AEBP1 knockdown-inhibited cell proliferation. Additionally, ACT001 blocks TGF-β-activated AEBP1/AKT signaling in GSCs. ACT001 exhibits antitumor activity either as a single agent or in combination with SHP099, which provides significant survival benefits for GSC xenograft tumor -bearing animals.

2020-09-11 | GSE157779 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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