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CUT&RUN studies comparing occupancy of MAX, MGA, MYC and L3MBTL2 occupancy in Empty vector and sgMGA transduced A549 lung adenocarcinoma cells

ABSTRACT: The goal of this study was to examine the genomic occupancy of MAX, MGA, MYC and L3MBTL2 in MGA depleted vs. control cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE161539 | GEO | 2020/11/16

REPOSITORIES: GEO

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Next-Generation Sequencing Facilitates Quantitative Analysis of Wild Type, Mga-/-, L3mbtl2-/- and Pcgf6-/- Embryonic Stem Cells Transcriptomes

Project description:Purpose: The goals of this study are to compare Mga-/-, L3mbtl2-/-, Pcgf6-/- and Wild type embryonic stem cells transcriptome profiling (RNA-seq) and compare the target genes of Mga, L3mbtl2 and Pcgf6.

2021-01-21 | GSE144141 | GEO

CUT&RUN studies comparing occupancy of MAX, MGA, MYC and L3MBTL2 occupancy in Empty vector and sgMGA transduced A549 lung adenocarcinoma cells

Project description:CUT&RUN studies comparing occupancy of MAX, MGA, MYC and L3MBTL2 occupancy in Empty vector and sgMGA transduced A549 lung adenocarcinoma cells

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CUT&RUN comparing the occupancy of MAX, MNT, MGA, MYC and RNA pol II Ser5 in a MAX null vs MAX reconstituted mouse SCLC line (mRPMaxKO)

Project description:The goal of this study was to compare the genomic occupancy of MAX, MNT, MGA and RNA pol II Ser5 in MAX restored versus MAX null SCLC (mRPMaxKO)

2020-06-06 | GSE146388 | GEO

Genomic occupancy of MYC and members of the PRC1.6 complex (MGA, E2F6, MAX, L3MBTL2) in MGA WT (Empty) and MGA depleted (sgMga) KrasG12D Trp53 -/- mouse lung cancer lines

Project description:Conventional crosslinked ChIP was performed on cell lines derived from control (Empty) and sgMga transduced tumors. We wanted to assess PRC1.6 member and MYC binding in the presence and absence of MGA.

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Genomic occupancy of MYC and members of the PRC1.6 complex (MGA, E2F6, MAX, L3MBTL2) in MGA WT (Empty) and MGA depleted (sgMga) KrasG12D Trp53 -/- mouse lung cancer lines

Project description:Genomic occupancy of MYC and members of the PRC1.6 complex (MGA, E2F6, MAX, L3MBTL2) in MGA WT (Empty) and MGA depleted (sgMga) KrasG12D Trp53 -/- mouse lung cancer lines

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MAX-mutant small cell lung cancers sustain impaired activities of the MGA-dependent ncPRC1

Project description:The MYC-axis is disrupted in cancer, mostly by activation of the MYC-oncogenes but also through inactivation of the MYC-partner, MAX, or of the MAX-partner, MGA, both also members of the polycomb repressive complex, ncPRC1.6. Here, we use genetically modified MAX-deficient small cell lung cancer (SCLC) cells and apply genome wide and proteomics analysis to study the tumor suppressor function of MAX. We find that MAX-mutant SCLCs classify as ASCL1-type and lack MYC-transcriptional activities. MAX-restitution triggers pro-differentiation expression profiles that shift when MAX and oncogenic MYC (HMYC/MAX) are co-expressed. Despite the ncPRC1.6 can be formed, the lack of MAX restricts global MGA-occupancy, selectively driving its recruitment towards E2F6-motifs. Conversely, MAX-restitution enhances MGA-occupancy and global gene repression of genes involved in different functionalities, including stem-cell and DNA repair/replication. Collectively, these findings reveal that MAX-mutant SCLCs have ASCL1-characteristics, are MYC-independent and their oncogenic features include a deficient ncPRC1.6-mediated gene repression.

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MAX-mutant small cell lung cancers exhibit impaired activities of MGA-dependent ncPRC1.6.

Project description:The MYC axis is commonly disrupted in cancer, mostly by activation of the MYC family of oncogenes, but also by genetic inactivation of MAX, the obligate partner of MYC, and of the MAX partner, MGA, both of which are members of the polycomb repressive complex, ncPRC1.6. While the oncogenic properties of the MYC family have been extensively studied, the tumor suppressor functions of MAX and MGA and the role of the MYC genes in MAX-mutant cells remain unclear. To address these knowledge gaps, we used chromatin immunoprecipitation, RNA-sequencing and mass spectrometry-based proteomic analysis in MAX-restituted and MYC oncogenic-transformed cell lines derived from human small cell lung cancer (SCLC), which is a high-grade neuroendocrine type of lung cancer. We found that MAX-mutant SCLC cells express ASCL1 and ASCL1-dependent targets, implying that these cells belong to the ASCL1-dependent group of SCLCs. In the absence of MAX, even after ectopic overexpression of MYC, we found no recruitment of MYC to the DNA. Furthermore, MAX reconstitution triggered pro-differentiation expression profiles that shifted when MAX and oncogenic MYC were co-expressed. Although ncPRC1.6 could be formed, the lack of MAX restricted global MGA occupancy, selectively driving its recruitment towards E2F6 motifs. Conversely, MAX restitution enhanced MGA occupancy and global gene repression of genes involved in different functions, including stem-cell and DNA repair/replication. Our data reveal that MAX-mutant SCLCs have ASCL1 characteristics, and are MYC-independent, and that their oncogenic features include deficient ncPRC1.6-mediated gene repression.

2021-09-22 | PXD017658 | Pride

SARS-CoV-2 Nsp6 damages Drosophila heart and mouse cardiomyocytes through MGA/MAX complex-mediated increased glycolysis

Project description:SARS-CoV-2 infection causes COVID-19, a severe acute respiratory disease associated with cardiovascular complications including long-term outcomes. The presence of virus in cardiac tissue of patients with COVID-19 suggests this is a direct, rather than secondary, effect of infection.Here, by expressing individual SARS-CoV-2 proteins in the Drosophila heart, we demonstrate interaction of virus Nsp6 with host proteins of the MGA/MAX complex (MGA, PCGF6 and TFDP1).

2022-10-04 | PXD036447 | Pride

RNA sequencing comparing human colon organoids transduced with Empty control vs. sgMGA (guide RNA targeting MGA)

Project description:The goal of this study was to compare expression profiles of normal colon organoids that have inactivated MGA compared to control organoids

2020-11-16 | GSE161543 | GEO

L3MBTL2 in HEK293 cells - ChIPseq

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