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

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

PROVIDER: PRJNA824355 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18672746_1.fastq.gz	Fastqsanger.gz
	SRR18672746_2.fastq.gz	Fastqsanger.gz
	SRR18672747_1.fastq.gz	Fastqsanger.gz
	SRR18672747_2.fastq.gz	Fastqsanger.gz
	SRR18672748_1.fastq.gz	Fastqsanger.gz

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

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

| PRJNA824352 | ENA

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: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

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

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

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

| PRJNA1129862 | ENA

MYC-MIZ1 protein interaction in germinal center.

Project description:MYC-MIZ1 protein interaction in germinal center.

| PRJNA530681 | ENA