Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HCP5 inhibits apoptosis via c-Myc transcriptional regulation mediated by UTP3 based chromatin-RNA-binding protein interaction

ABSTRACT: HCP5 inhibits apoptosis via c-Myc transcriptional regulation mediated by UTP3 based chromatin-RNA-binding protein interaction

PROVIDER: PRJNA824352 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18653042_1.fastq.gz	Fastqsanger.gz
	SRR18653042_2.fastq.gz	Fastqsanger.gz
	SRR18653043_1.fastq.gz	Fastqsanger.gz
	SRR18653043_2.fastq.gz	Fastqsanger.gz
	SRR18653044_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

MYCMI-7 - a small MYC-binding compound that inhibits MYC:MAX interaction and tumor growth in a MYC-dependent manner

Project description:Deregulated expression of MYC family oncogenes occurs frequently in human cancer and is often associated with aggressive disease and poor prognosis. While MYC is a highly warranted target, it has been considered “undruggable”, and no specific anti-MYC drugs are available in the clinic. We recently identified molecules named MYCMIs that inhibit the interaction between MYC and its essential partner MAX. Here we show that one of these, MYCMI-7, efficiently and selectively inhibits MYC:MAX and MYCN:MAX interactions in cells, binds directly to recombinant MYC and reduces MYC-driven transcription. In addition, MYCMI-7 induces degradation of MYC and MYCN proteins. MYCMI-7 potently induces growth arrest/apoptosis in tumor cells in a MYC/MYCN- dependent manner and downregulates the MYC pathway on a global level as determined by RNA-seq. Sensitivity to MYCMI-7 correlates with MYC expression in a panel of 60 tumor cell lines and MYCMI-7 shows high efficacy towards a collection of patient- derived primary glioblastoma and acute myeloid leukemia (AML) ex vivo cultures. Importantly, a variety of normal cells become G1 arrested without signs of apoptosis upon MYCMI-7 treatment. Finally, in mouse tumor models of MYC-driven AML, breast cancer and MYCN-amplified neuroblastoma, treatment with MYCMI-7 downregulates MYC/MYCN, inhibits tumor growth and prolongs survival through apoptosis with little side effects. In conclusion, MYCMI-7 is a potent and selective MYC inhibitor that is highly relevant for the development into clinically useful drugs for treatment of MYC-driven cancer.

2023-03-08 | GSE197062 | GEO

HCP5 inhibits apoptosis via c-Myc transcriptional regulation mediated by UTP3 based chromatin-RNA-binding protein interaction [RNA-Seq]

Project description:HCP5 inhibits apoptosis via c-Myc transcriptional regulation mediated by UTP3 based chromatin-RNA-binding protein interaction [RNA-Seq]

| PRJNA823918 | ENA

HCP5 inhibits apoptosis via c-Myc transcriptional regulation mediated by UTP3 based chromatin-RNA-binding protein interaction [ATAC-Seq]

Project description:HCP5 inhibits apoptosis via c-Myc transcriptional regulation mediated by UTP3 based chromatin-RNA-binding protein interaction [ATAC-Seq]

| PRJNA824355 | ENA

HCP5 inhibits apoptosis via c-Myc transcriptional regulation mediated by UTP3 based chromatin-RNA-binding protein interaction [ATAC-Seq]

Project description:This study demonstrates that HCP5/UTP3/c-Myc/VAMP3 axis plays important role in inhibition of cancer cell apoptosis and HCP5 can be targeted to contribute to cell apoptosis induced by cytotoxic agents.

2022-10-26 | GSE200373 | GEO

HCP5 inhibits apoptosis via c-Myc transcriptional regulation mediated by UTP3 based chromatin-RNA-binding protein interaction [RNA-Seq]

2022-10-26 | GSE200270 | GEO

MYCMI-7 - a small MYC-binding compound that inhibits MYC:MAX interaction and tumor growth in a MYC-dependent manner

Project description:MYCMI-7 - a small MYC-binding compound that inhibits MYC:MAX interaction and tumor growth in a MYC-dependent manner

| PRJNA808742 | ENA

MYC sensitises cells to apoptosis by driving energetic demand

Project description:The MYC oncogene is a potent driver of growth and proliferation but also sensitises cells to apoptosis, which limits its oncogenic potential. MYC induces several biosynthetic programmes and primary cells overexpressing MYC are highly sensitive to glutamine withdrawal suggesting that MYC-induced sensitisation to apoptosis may be due to an imbalance of metabolic/energetic supply and demand. Here we show that MYC elevates global transcription and translation, even in the absence of glutamine, revealing metabolic demand without corresponding supply. Glutamine withdrawal from MRC-5 fibroblasts depleted key TCA cycle metabolites and, in combination with MYC activation, led to AMP accumulation and nucleotide catabolism indicative of energetic stress. Further analyses revealed that glutamine supports viability through TCA cycle energetics rather than asparagine biosynthesis and that TCA cycle inhibition confers tumour suppression on MYC- driven lymphoma in vivo. In summary, glutamine supports the viability of MYC- overexpressing cells through an energetic rather than a biosynthetic mechanism.

2022-08-11 | PXD034517 | Pride

N-acetylcysteine and Vitamin C stimulate MYC binding to EGR1 and selectively stimulate apoptosis in B cell lymphoma

Project description:Refractory and relapsed B cell lymphomas are often driven by MYC, a difficult-to-target oncogene due to its central role in normal transcription. Here we report that N-acetylcysteine (NAC) and vitamin C (VitC)—in doses that reduce reactive oxygen species levels levels—trigger apoptosis in human B lymphoma cells with high MYC expression. Intraperitoneal NAC and VitC injections dose-dependently reduced tumor growth in xenograft experiments, and combined NAC/VitC administration stopped tumor growth. Knockdown of MYC restored tumor growth in the presence of NAC and VitC and switching-on MYC expression in B cells rendered them sensitive to the compounds. The compounds stimulated MYC binding to Early growth response protein 1 (EGR1)—an interaction found to require Cys132 of MYC—which reduced MYC binding to promotors of cell cycle genes and increased binding to apoptotic genes; and thus, switched MYC’s transcriptional output from cell cycle to apoptosis gene expression. Short-term combined NAC/VitC administration into λMYC transgenic mice, an endogenous mouse model of B cell lymphoma, after tumor onset increased survival fourfold; and life-long oral administration of NAC and VitC stimulated apoptosis and reduced B cell progenitors in the spleen and measurably increased survival. The results provide a rationale with mechanistic understanding for evaluating the therapeutic efficacy of NAC and VitC in patients with MYC-driven B cell lymphoma.

2023-08-01 | GSE199843 | GEO

HCP5 inhibits apoptosis via c-Myc transcriptional regulation mediated by UTP3 based chromatin-RNA-binding protein interaction

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

2022-10-26 | GSE200375 | GEO

Luteoloside inhibits proliferation, induces apoptosis and differentiation via β-catenin/c-Myc axis in acute myeloid leukemia

Project description:Background: Acute myeloid leukemia (AML) is the most common leukemia in adults, that has a poor prognosis due in part to low response to treatment and high recurrence. And drugs commonly used in conventional treatment strategies often cause serious side-effects. Purpose: To investigate the high efficacy and low toxicity of luteoloside on AML and explore its mechanism of action. Methods:The proliferation of AML cells treated with different concentrations of luteoloside was assessed by the CCK-8 assay and colony formation assay, and apoptosis and differentiation were detected by flow cytometry. RNA-Seq analysis and western blotting were performed to explore the mechanism by which luteoloside exerted anti-AML effects. The patient-derived xenografts (PDX) model was established to assess anti-AML effect of luteoloside in vivo, and construction of an orthotopic AML mouse model explored the combination therapy of luteoloside and cytarabine. Results: Herein, we found that luteoloside could dramatically impair the proliferation and clonogenic capacity of AML cells and induce S phase arrest associated with decrease of Cyclin D1 and increase of Cyclin A2. Furthermore, luteoloside induced apoptosis and promoted differentiation of AML cells. Activation of Wnt/β-catenin signaling by GSK3β inhibitor LiCl reversed the inhibitory effect of luteoloside on AML cell proliferation, apoptosis, and differentiation, due to β-catenin entering into nucleus and reducing the expression of c-Myc. Luteoloside significantly reduced the transplantation rate of primary AML cells in PDX model, and the combination of luteoloside and cytarabine showed a synergistic anti-AML effect in orthotopic AML model. Conclusion: Our findings demonstrate that luteoloside inhibits proliferation, induces apoptosis and differentiation of AML cells via suppression of β-catenin/c-Myc axis, suggesting that luteoloside can be developed as a potential anti-AML drug.

2024-07-04 | GSE271106 | 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