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MYC couples SWI/SNF and metabolic reprogramming to sustain minimal residual disease in mTORC1-activated cancer cells

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

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE270779 | GEO | 2025/06/10

REPOSITORIES: GEO

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MYC couples SWI/SNF and metabolic reprogramming to sustain minimal residual disease in mTORC1-activated cancer cells [WES]

Project description:Therapeutics blocking PI3K-mTORC1 are commonly used for tumor treatment, and at times achieve major responses, yet minimal residual disease (MRD) persists, leading to tumor relapse. We examined the MRD models established both in vitro (Rapamycin persistent, RP) and in vivo after mTORC1 inhibition. All RP/MRD cell lines showed complete growth and signaling insensitivity to rapamycin but variable sensitivity to bi-steric mTORC1 inhibitors. MTORS2035 mutations were identified in 4 of 7 RP cell lines. Multi-omic analysis identified a pronounced shift to oxidative phosphorylation and away from glycolysis in all RP/MRD models, with increased mitochondrial number and function. MYC and SWI/SNF expression were greatly enhanced. Both the SWI/SNF inhibitor AU-15330 and the Complex I inhibitor of oxidative phosphorylation IACS-010759 showed pronounced synergy with bi-steric mTORC1 inhibitors to cause cuproptotic cell death in RP/MRD cells, suggesting these combinations as a potential patient treatment strategy for rapalog resistance.

2025-06-10 | GSE270778 | GEO

MYC couples SWI/SNF and metabolic reprogramming to sustain minimal residual disease in mTORC1-activated cancer cells [RNA-seq]

2025-06-10 | GSE270777 | GEO

MYC couples SWI/SNF and metabolic reprogramming to sustain minimal residual disease in mTORC1-activated cancer cells [CUT&RUN, ATAC-seq]

2025-06-10 | GSE270774 | GEO

MYC couples SWI/SNF and metabolic reprogramming to sustain minimal residual disease in mTORC1-activated cancer cells

Project description:MYC couples SWI/SNF and metabolic reprogramming to sustain minimal residual disease in mTORC1-activated cancer cells

| PRJNA1128156 | ENA

MYC couples SWI/SNF and metabolic reprogramming to sustain minimal residual disease in mTORC1-activated cancer cells [WES]

Project description:MYC couples SWI/SNF and metabolic reprogramming to sustain minimal residual disease in mTORC1-activated cancer cells [WES]

| PRJNA1128160 | ENA

MYC couples SWI/SNF and metabolic reprogramming to sustain minimal residual disease in mTORC1-activated cancer cells [RNA-seq]

Project description:MYC couples SWI/SNF and metabolic reprogramming to sustain minimal residual disease in mTORC1-activated cancer cells [RNA-seq]

| PRJNA1128159 | ENA

MYC couples SWI/SNF and metabolic reprogramming to sustain minimal residual disease in mTORC1-activated cancer cells [CUT&RUN, ATAC-seq]

Project description:MYC couples SWI/SNF and metabolic reprogramming to sustain minimal residual disease in mTORC1-activated cancer cells [CUT&RUN, ATAC-seq]

| PRJNA1128150 | ENA

Role of SWI/SNF in acute leukemia maintenance and enhancer-mediated Myc regulation.

Project description:Cancer cells frequently depend on chromatin regulatory activities to maintain a malignant phenotype. Here, we show that leukemia cells require the mammalian SWI/SNF chromatin remodeling complex for their survival and aberrant self-renewal potential. While Brg1, an ATPase subunit of SWI/SNF, is known to suppress tumor formation in several cell types, we found that leukemia cells instead rely on Brg1 to support their oncogenic transcriptional program, which includes Myc as one of its key targets. To account for this context-specific function, we identify a cluster of lineage-specific enhancers located 1.7 Mb downstream from Myc that are occupied by SWI/SNF as well as the BET protein Brd4. Brg1 is required at these distal elements to maintain transcription factor occupancy and for long-range chromatin looping interactions with the Myc promoter. Notably, these distal Myc enhancers coincide with a region that is focally amplified in ?3% of acute myeloid leukemias. Together, these findings define a leukemia maintenance function for SWI/SNF that is linked to enhancer-mediated gene regulation, providing general insights into how cancer cells exploit transcriptional coactivators to maintain oncogenic gene expression programs.

| S-EPMC3877755 | biostudies-literature

In vivo analysis reveals that ATP-hydrolysis couples remodeling to SWI/SNF release from chromatin.

Project description:ATP-dependent chromatin remodelers control the accessibility of genomic DNA through nucleosome mobilization. However, the dynamics of genome exploration by remodelers, and the role of ATP hydrolysis in this process remain unclear. We used live-cell imaging of Drosophila polytene nuclei to monitor Brahma (BRM) remodeler interactions with its chromosomal targets. In parallel, we measured local chromatin condensation and its effect on BRM association. Surprisingly, only a small portion of BRM is bound to chromatin at any given time. BRM binds decondensed chromatin but is excluded from condensed chromatin, limiting its genomic search space. BRM-chromatin interactions are highly dynamic, whereas histone-exchange is limited and much slower. Intriguingly, loss of ATP hydrolysis enhanced chromatin retention and clustering of BRM, which was associated with reduced histone turnover. Thus, ATP hydrolysis couples nucleosome remodeling to remodeler release, driving a continuous transient probing of the genome.

| S-EPMC8352592 | biostudies-literature

Multiple interactions of the oncoprotein transcription factor MYC with the SWI/SNF chromatin remodeler.

Project description:The SNF5 subunit of the SWI/SNF chromatin remodeling complex has been shown to act as a tumor suppressor through multiple mechanisms, including impairing the ability of the oncoprotein transcription factor MYC to bind chromatin. Beyond SNF5, however, it is unknown to what extent MYC can access additional SWI/SNF subunits or how these interactions affect the ability of MYC to drive transcription, particularly in SNF5-null cancers. Here, we report that MYC interacts with multiple SWI/SNF components independent of SNF5. We show that MYC binds the pan-SWI/SNF subunit BAF155 through the BAF155 SWIRM domain, an interaction that is inhibited by the presence of SNF5. In SNF5-null cells, MYC binds with remaining SWI/SNF components to essential genes, although for a purpose that is distinct from chromatin remodeling. Analysis of MYC-SWI/SNF target genes in SNF5-null cells reveals that they are associated with core biological functions of MYC linked to protein synthesis. These data reveal that MYC can bind SWI/SNF in an SNF5-independent manner and that SNF5 modulates access of MYC to core SWI/SNF complexes. This work provides a framework in which to interrogate the influence of SWI/SNF on MYC function in cancers in which SWI/SNF or MYC are altered.

| S-EPMC8141032 | biostudies-literature

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