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MAX inactivation deregulates the MYC network and induces neuroendocrine neoplasia in multiple tissues [RNA-seq]

ABSTRACT: MAX inactivation deregulates the MYC network and induces neuroendocrine neoplasia in multiple tissues [RNA-seq]

PROVIDER: PRJNA1209547 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31968726.fastq.gz	Fastqsanger.gz
	SRR31968727.fastq.gz	Fastqsanger.gz
	SRR31968728.fastq.gz	Fastqsanger.gz
	SRR31968729.fastq.gz	Fastqsanger.gz
	SRR31968730.fastq.gz	Fastqsanger.gz

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MAX inactivation deregulates the MYC network and induces neuroendocrine neoplasia in multiple tissues [ChIP-seq]

Project description:The MYC transcription factor requires MAX for DNA binding and widespread activation of gene expression in both normal and neoplastic cells. Surprisingly, inactivating mutations in MAX are associated with a subset of neuroendocrine cancers including pheochromocytoma, pituitary adenoma and small cell lung cancer. Neither the extent nor the mechanisms of MAX tumor suppression are well understood. Deleting Max across multiple mouse neuroendocrine tissues, we find Max inactivation alone produces pituitary adenomas while Max inactivation loss cooperates with Rb1/Trp53 loss to accelerate medullary thyroid C-cell and pituitary adenoma development. In the thyroid tumor cell lines, MAX loss triggers a striking shift in genomic occupancy by other members of the MYC network (MNT, MLX, MondoA) supporting metabolism, survival and proliferation of neoplastic neuroendocrine cells. Our work reveals MAX as a broad suppressor of neuroendocrine tumorigenesis through its ability to maintain a balance of genomic occupancies among the diverse transcription factors in the MYC network.

2025-03-15 | GSE286458 | GEO

MAX inactivation deregulates the MYC network and induces neuroendocrine neoplasia in multiple tissues [RNA-seq]

2025-03-15 | GSE286461 | GEO

MAX inactivation deregulates the MYC network and induces neuroendocrine neoplasia in multiple tissues [ChIP-seq]

Project description:MAX inactivation deregulates the MYC network and induces neuroendocrine neoplasia in multiple tissues [ChIP-seq]

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Proteogenomic profiling of thymic and pulmonary neuroendocrine neoplasia.

Project description:This study represents a proteogenomic resource for thymic and pulmonary neuroendocrine neoplasia (NEN) and provides a proteomgenomic diagnostic signature for classification of low and high grade NEN.

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Proteogenomic profiling of thymic and pulmonary neuroendocrine neoplasia.

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Proteogenomic profiling of thymic and pulmonary neuroendocrine neoplasia.

Project description:Proteogenomic profiling of thymic and pulmonary neuroendocrine neoplasia.

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Proteomic Analysis of Canine Hepatobiliary Neuroendocrine Neoplasms

Project description:Neuroendocrine neoplasms of the gallbladder and liver occur rarely in dogs and humans. A recent reclassification of human neuroendocrine neoplasms by the World Health Organization has refined categorization of these tumors by morphology, replicative indices, and molecular signatures. In humans, these factors correlate with survival outcomes. Improved characterization of these tumors is needed in dogs to identify diagnostic biomarkers and determine therapeutic strategies. To achieve this objective, the proteome of 3 canine hepatobiliary neoplasms was compared to normal canine adrenal and liver tissue from formalin-fixed paraffin-embedded samples. Thirty-two upregulated and 121 downregulated differentially expressed proteins were identified in the hepatobiliary neuroendocrine neoplasm samples. Among the upregulated proteins is galectin-1, a multivalent carbohydrate binding protein known to play a role in lung and pancreatic neuroendocrine neoplasia development and progression in humans. Drugs targeting the galectin family have shown promise as anticancer therapeutics in cervical cancer, prostate cancer, lung and pancreatic neuroendocrine neoplasia in human medicine. Galectin-1 may represent a novel treatment target in hepatobiliary neuroendocrine neoplasia in both humans and dogs.

2023-03-11 | PXD028822 | Pride

Inactivation of mitochondrial MUL1 E3 ubiquitin ligase deregulates mitophagy and prevents diet-induced obesity in mice

Project description:Inactivation of mitochondrial MUL1 E3 ubiquitin ligase deregulates mitophagy and prevents diet-induced obesity in mice

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Global transcriptional responses to KI-MS2-008 treatment and Myc inactivation via doxycycline addition

Project description:The Myc/Max heterodimer has crucial roles in normal cellular processes such as cell proliferation, metabolism, apoptosis, and differentiation, but its activity is often deregulated in a majority of human cancers. In an effort to explore alternative modes of Myc perturbation, we identified KI-MS2-008 as a small molecule that binds Max and modulates Myc-driven transcription, and in some cellular contexts, KI-MS2-008 treatment leads to a decrease in c-Myc protein levels. As the Myc/Max heterodimer controls many cellular processes, we expected that treatment with this small molecule would cause changes in the transcriptome. We found that treatment with 10 µM KI-MS2-008 resulted in global alterations in the transcriptome, mimicking direct Myc inactivation with doxycycline in P493-6, a B cell line with a Tet-Off system for c-Myc expression. We also discovered enrichment of various Myc target gene sets in the genes downregulated in response to KI-MS2-008 treatment in P493-6 cells. This trend was also observed in ST486 cells, but not in P3HR1 cells, which were chosen as non-engineered B cell lines that were sensitive and insensitive, respectively, toward KI-MS2-008 in cell viability assays.

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CUT&RUN comparing occupancy of MAX, MNT, MYC in MAX WT and KO B220+ cells

Project description:The goal of this study was to genomic occupancy of MAX, MNT, MYC and E2F1 in B cells in the presence and absence of transcription factor MAX Although MAX is regarded as an obligate dimerization partner for MYC, its function in normal development and neoplasia is poorly defined. We show that B-cell specific deletion of Max has a modest effect on B-cell development but completely abrogates E -Myc driven lymphomagenesis. While Max loss only affects a few hundred genes in normal B cells, it leads to the global downregulation of Myc-activated genes in premalignant E -Myc cells. We show that the balance between MYC-MAX and MNT-MAX interactions in B cells shifts in pre-malignant B cells towards a MYC driven transcriptional program. Moreover, we find that MAX loss leads to a significant reduction in MYC protein levels and downregulation of direct transcriptional targets, including regulators of MYC stability. This phenomenon is also observed in multiple cell lines treated with MYC-MAX dimerization inhibitors. Our work uncovers a layer of Myc autoregulation critical for lymphomagenesis yet partly dispensable for normal development.

2019-06-20 | GSE132967 | GEO

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