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MTSS1 Suppresses Expansion and Activity of Mammary Tumor-initiating Cells by Mediating P65 Ubiquitination and Degradation

ABSTRACT: MTSS1 Suppresses Expansion and Activity of Mammary Tumor-initiating Cells by Mediating P65 Ubiquitination and Degradation

PROVIDER: PRJNA522687 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8581330_1.fastq.gz	Fastqsanger.gz
	SRR8581330_2.fastq.gz	Fastqsanger.gz
	SRR8581327_1.fastq.gz	Fastqsanger.gz
	SRR8581327_2.fastq.gz	Fastqsanger.gz
	SRR8581328_1.fastq.gz	Fastqsanger.gz

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MTSS1 Suppresses Expansion and Activity of Mammary Tumor-initiating Cells by Mediating P65 Ubiquitination and Degradation

Project description:We conduct transcriptome comparison of control and Mtss1-overexpressed Py8119 cells to gain genomic insights on the biological processes that Mtss1 is involved in breast cancer cells. Through unsupervised cluster analysis of differentially expressed genes (DEGs), we found 1661 genes were significantly changed in Mtss1 cells. Single Site Analysis and Gene Set Enrichment Analysis show that Mtss1 downregualted numerous NF-κB targeted genes.

2019-10-29 | GSE126606 | GEO

MTSS1 Suppresses NF-kB Activity in Lung Adenocarcinoma through Repression of RelA/p65 Phosphorylation

Project description:Metastasis suppressor 1 (MTSS1) is a 755 amino acid protein found in the cell cytoplasm which binds to actin and promotes cytoskeleton organization and is a known suppressor of lung adenocarcinoma metastasis This study demonstrated that preservation of MTSS1 protein expression in lung adenocarcinoma was associated with a 20% 5-year survival advantage in patients. Furthermore, overexpression of MTSS1 was found to reduce metastasis and disease progression in an in-vivo orthotopic lung adenocarcinoma mouse model. Nuclear factor kappa B (NF-kB), an important nuclear transcription factor, has been shown to be constitutively active in lung adenocarcinoma and strongly associated with the development of metastasis. The NF-kB RelA/p65 subunit is involved in NF-kB heterodimer formation and subsequent nuclear translocation leading to activation of NF-kB responsive gene transcription. Phosphorylation and acetylation of p65 are critical post-translational modifications required for NF-kB activation. In this study, we demonstrate that MTSS1 expression leads to decreased NF-κB mediated gene transcription through inhibition of p65 phosphorylation. These findings uncover a novel mechanism through which MTSS1 may regulate lung adenocarcinoma metastasis by impairment of NF-κB regulated gene transcription.

2024-07-07 | GSE179644 | GEO

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Project description:p65

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MTSS1 Suppresses NF-kB Activity in Lung Adenocarcinoma through Repression of RelA/p65 Phosphorylation

Project description:MTSS1 Suppresses NF-kB Activity in Lung Adenocarcinoma through Repression of RelA/p65 Phosphorylation

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Effects of p65 palmitoylation on gene expression when overexpressing vector or p65 WT or p65 2CS in p65 knockout 293A cells combined with TNFα treatment

Project description:Nuclear factor kappa B (NF-κB) is a central regulator of inflammation, infection, and immunity pathways and is often dysregulated in autoimmune diseases, inflammatory disorders, and cancers. However, the mechanisms by which different stimuli, including cellular metabolism, modulate NF-κB activation remain unclear. Here, we report that RelA ( p65), a major component of NF-κB, is S-palmitoylated at cysteine 197 and 206 by directly reacting with palmitoyl-CoA. Autopalmitoylation of p65 promotes its nuclear localization and p65-p50 complex formation, thereby enhancing NF-κB transcriptional activities. Furthermore, p65 palmitoylation upregulates RelB expression and promotes non-canonical NF-κB complex formation, further amplifying pathway activation. We also demonstrate that a high-fat diet could enhance p65 palmitoylation and correlate with an increased cytokine production in mouse tissues. These results reveal that lipid metabolism might directly regulate NF-κB activity and suggest that targeting p65 auto-palmitoylation could be a potential therapeutic strategy for diseases with deregulated NF-κB pathway.

2025-01-17 | GSE286561 | GEO

FBXO44 Regulates Rac1 Spatiotemporal Dynamics: An Exploitable Therapeutic Vulnerability for Actin Cytoskeleton-Targeted Treatment in Gastric Cancer

Project description:The dynamic homeostasis of the cytoskeleton represents a critical vulnerability in tumor cells, yet the molecular mechanisms governing this equilibrium remain elusive. In the present study, we identify FBXO44 as a crucial regulator of Rac1 nucleocytoplasmic shuttling through its interaction with MTSS1. In gastric cancer (GC), FBXO44 orchestrates dual ubiquitination programs on MTSS1: K63-linked polyubiquitination promotes Rac1 nuclear translocation to drive cytoskeletal remodeling, whereas K11-linked modification triggers MTSS1 proteasomal degradation to restrict Rac1 nuclear trafficking. Structural analysis reveals that FBXO44 engages MTSS1 through distinct domains, dynamically balancing these opposing ubiquitination events through precise control MTSS1 protein levels, thereby calibrating actin cytoskeletal dynamics. Clinically, this regulatory axis maintains an oncogenic equilibrium-FBXO44 overexpression correlates with Rac1 signaling activation in progressive GC patients. Therapeutically, pharmacological disruption of this balance using the novel inhibitor DQ2405 achieves dual anti-tumor effects: suppressing tumor growth and metastatic capacity. Our findings establish FBXO44-mediated Rac1 spatiotemporal control as a druggable strategy for actin-cytoskeleton targeted therapy, providing both mechanistic insights into cytoskeletal homeostasis and a translational framework for GC treatment.

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Project description:In effort to develop methodology for targeted top down mass spectrometry of NF kappa B p65 from human cells, we evaluated the utility of HaloTag for purification and analysis of recombinant protein. During our study, two datasets of bottom up LC-MS/MS were generated: one from in-gel digestion of the predominant band following p65-HaloTag purification, another from in-solution digestion of all the proteins present in a p65-HaloTag purification. p65-HaloTag copurifying proteins identified in our datasets include the known interactors c-Rel, NF-kappaB p105, NF-kappaB p100, and NF-kappaB inhibitor beta. Over 100 proteins were identified by at least two peptides using a Mascot ion cut-off score of 30.

2018-10-19 | PXD001932 | Pride

Tripartite motif 8 promotes hepatocellular carcinogenesis by mediating ubiquitination and degradation of hepatocyte nuclear factor 1α

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RNA Sequencing looking at differential gene expression between p65+/+ and p65-/- mouse embryonic fibroblasts (MEFs)

Project description:We look at differential gene expression between immortalized p65+/+ and p65-/- MEFs to identify potential NF-kB regulated genes which when grouped based on biological function indicates candidates involved in protecting p65+/+ cells from macrophage-mediated killing

2017-10-01 | GSE101092 | GEO

Effects of p65 palmitoylation on gene expression when overexpressing vector or p65 WT or p65 2CS in p65 knockout 293A cells combined with TNFα treatment

Project description:Effects of p65 palmitoylation on gene expression when overexpressing vector or p65 WT or p65 2CS in p65 knockout 293A cells combined with TNFα treatment

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