Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Enhancer remodeling activates Notch signaling to confer chemoresistance in advanced nasopharyngeal carcinoma

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE214026 | GEO | 2025/09/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Enhancer remodeling activates NOTCH3 signaling to confer chemoresistance in advanced nasopharyngeal carcinoma.

Project description:Acquired resistance to chemotherapy is one of the major causes of mortality in advanced nasopharyngeal carcinoma (NPC). However, effective strategies are limited and the underlying molecular mechanisms remain elusive. In this study, through transcriptomic profiling analysis of 23 tumor tissues, we found that NOTCH3 was aberrantly highly expressed in chemoresistance NPC patients, with NOTCH3 overexpression being positively associated with poor clinical outcome. Mechanistically, using an established NPC cellular model, we demonstrated that enhancer remodeling driven aberrant hyperactivation of NOTCH3 in chemoresistance NPC. We further showed that NOTCH3 upregulates SLUG to induce chemo-resistance of NPC cells and higher expression of SLUG have poorer prognosis. Genetic or pharmacological perturbation of NOTCH3 conferred chemosensitivity of NPC in vitro and overexpression of NOTCH3 enhanced chemoresistance of NPC in vivo. Together, these data indicated that genome-wide enhancer reprogramming activates NOTCH3 to confer chemoresistance of NPC, suggesting that targeting NOTCH3 may provide a potential therapeutic strategy to effectively treat advanced chemoresistant NPC.

| S-EPMC10415329 | biostudies-literature

Enhancer remodeling activates Notch signaling to confer chemoresistance in advanced nasopharyngeal carcinoma [RNA-Seq]

Project description:Acquired resistance to chemotherapy is one of the major causes of mortality in advanced nasopharyngeal carcinoma (NPC). However, effective strategies are limited and the underlying molecular mechanisms remain elusive. Using an established NPC cellular model, we demonstrated that the acquisition of chemoresistance was accompanied by massive enhancer remodeling, resulting in aberrant hyperactivation of Notch signaling pathway in NPC. Transcriptomic profiling analysis showed that hyperactivity of Notch signaling pathway was associated with chemoresistance in advanced NPC patients. In addition, overexpression of Notch3-slug axis was correlated with relapses and metastasis of NPC. Importantly, we showed that genetic or pharmacological perturbation of Notch3 could overcome the chemoresistance of NPC in both in vitro and in vivo models. Together, our study indicated that genome-wide enhancer reprogramming activates Notch signaling pathway to confer chemoresistance of NPC, suggesting that targeting Notch3 could provide a potential therapeutic strategy to effectively treat advanced chemoresistant NPC.

2025-09-21 | GSE214025 | GEO

Enhancer remodeling activates Notch signaling to confer chemoresistance in advanced nasopharyngeal carcinoma [ChIP-Seq]

Project description:Acquired resistance to chemotherapy is one of the major causes of mortality in advanced nasopharyngeal carcinoma (NPC). However, effective strategies are limited and the underlying molecular mechanisms remain elusive. Using an established NPC cellular model, we demonstrated that the acquisition of chemoresistance was accompanied by massive enhancer remodeling, resulting in aberrant hyperactivation of Notch signaling pathway in NPC. Transcriptomic profiling analysis showed that hyperactivity of Notch signaling pathway was associated with chemoresistance in advanced NPC patients. In addition, overexpression of Notch3-slug axis was correlated with relapses and metastasis of NPC. Importantly, we showed that genetic or pharmacological perturbation of Notch3 could overcome the chemoresistance of NPC in both in vitro and in vivo models. Together, our study indicated that genome-wide enhancer reprogramming activates Notch signaling pathway to confer chemoresistance of NPC, suggesting that targeting Notch3 could provide a potential therapeutic strategy to effectively treat advanced chemoresistant NPC. 1. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq ) for H3K27Ac, H3K4me3 in 5-8F P and 5-8F R cells

2025-09-21 | GSE214023 | GEO

Enhancer remodeling activates Notch signaling to confer chemoresistance in advanced nasopharyngeal carcinoma

Project description:Enhancer remodeling activates Notch signaling to confer chemoresistance in advanced nasopharyngeal carcinoma

| PRJNA883647 | ENA

Enhancer remodeling activates Notch signaling to confer chemoresistance in advanced nasopharyngeal carcinoma [ChIP-Seq]

Project description:Enhancer remodeling activates Notch signaling to confer chemoresistance in advanced nasopharyngeal carcinoma [ChIP-Seq]

| PRJNA883652 | ENA

Enhancer remodeling activates Notch signaling to confer chemoresistance in advanced nasopharyngeal carcinoma [RNA-Seq]

Project description:Enhancer remodeling activates Notch signaling to confer chemoresistance in advanced nasopharyngeal carcinoma [RNA-Seq]

| PRJNA883653 | ENA

CD146 regulates the stemness and chemoresistance of hepatocellular carcinoma via JAG2-NOTCH signaling.

Project description:CD146 plays a key role in cancer progression and metastasis. Cancer stem cells (CSCs) are responsible for tumor initiation, drug resistance, metastasis, and recurrence. In this study, we explored the role of CD146 in the regulation of liver CSCs. Here, we demonstrated that CD146 was highly expressed in liver CSCs. CD146 overexpression promoted the self-renewal ability and chemoresistance of Hepatocellular Carcinoma (HCC) cells in vitro and tumorigenicity in vivo. Inversely, knockdown of CD146 restrained these abilities. Mechanistically, CD146 activated the NF-κB signaling to up-regulate JAG2 expression and activated the Notch signaling, which resulted in increased stemness of HCC. Furthermore, JAG2 overexpression restored the Notch signaling activity, the stemness, and chemotherapeutic resistance caused by CD146 knockdown. These results demonstrated that CD146 positively regulates HCC stemness by activating the JAG2-NOTCH signaling. Combined targeting of CD146 and JAG2 may represent a novel therapeutic strategy for HCC treatment.

| S-EPMC11876685 | biostudies-literature

SWI/SNF chromatin remodeling controls Notch-responsive enhancer accessibility.

Project description:Notch signaling plays a key role in many cell fate decisions during development by directing different gene expression programs via the transcription factor CSL, known as Su(H) in Drosophila Which target genes are responsive to Notch signaling is influenced by the chromatin state of enhancers, yet how this is regulated is not fully known. Detecting a specific increase in the histone variant H3.3 in response to Notch signaling, we tested which chromatin remodelers or histone chaperones are required for the changes in enhancer accessibility to Su(H) binding. We show a crucial role for the Brahma SWI/SNF chromatin remodeling complex, including the actin-related BAP55 subunit, in conferring enhancer accessibility and enabling the transcriptional response to Notch activity. The Notch-responsive regions have high levels of nucleosome turnover which depend on the Brahma complex, increase in magnitude with Notch signaling, and primarily involve histone H3.3. Together these results highlight the importance of SWI/SNF-mediated nucleosome turnover in rendering enhancers responsive to Notch.

| S-EPMC6500979 | biostudies-literature

Melatonin reverses nasopharyngeal carcinoma cisplatin chemoresistance by inhibiting the Wnt/β-catenin signaling pathway.

Project description:Cisplatin (DDP)-based concurrent chemo-radiotherapy is a standard approach to treat locoregionally advanced nasopharyngeal carcinoma (NPC). However, many patients eventually develop recurrence and/or distant metastasis due to chemoresistance. In this study, we aimed to elucidate the effects of melatonin on DDP chemoresistance in NPC cell lines in vitro and vivo, and we explored potential chemoresistance mechanisms. We found that DDP chemoresistance in NPC cells is mediated through the Wnt/β-catenin signaling pathway. Melatonin not only reversed DDP chemoresistance, but also enhanced DDP antitumor activity by suppressing the nuclear translocation of β-catenin, and reducing expression of Wnt/β-catenin response genes in NPC cells. In vivo, combined treatment with DDP and melatonin reduced tumor burden to a greater extent than single drug-treatments in an orthotopic xenograft mouse model. Our findings provide novel evidence that melatonin inhibits the Wnt/β-catenin pathway in NPC, and suggest that melatonin could be applied in combination with DDP to treat NPC.

| S-EPMC7138577 | biostudies-literature

Notch signaling and bone remodeling.

Project description:Notch signaling plays context-dependent roles in the development and maintenance of many cell types and tissues in mammals. In the skeleton, both osteoblasts and osteoclasts require Notch signaling for proper differentiation and function, and the specific roles of Notch are dependent on the differentiation status of the cell. The recent discovery of activating NOTCH2 mutations as the cause of Hajdu-Cheney syndrome has highlighted the significance of Notch signaling in human bone physiology.

| S-EPMC3645324 | biostudies-literature

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