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IP-MS of LSD1 and ER in treated Breast cancer cells

ABSTRACT: These proteomic data were produced in order to assess the effect of drug 3324, a pan-lysine demethylase inhibitor, on the estrogen receptor (ER) and Lysine Demethylase1 (LSD1)protein interaction networks.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Breast Epithelium, Cell Culture

DISEASE(S): Breast Cancer

SUBMITTER: Tommaso De Marchi

LAB HEAD: Lucia Altucci

PROVIDER: PXD012781 | Pride | 2021-09-08

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	20180301_Human_CnI_sp.fasta	Fasta
	TDM_H1801_268.raw	Raw
	TDM_H1801_270.raw	Raw
	TDM_H1801_272.raw	Raw
	TDM_H1801_286.raw	Raw

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Publications

Regulatory Interplay between miR-181a-5p and Estrogen Receptor Signaling Cascade in Breast Cancer.

Benedetti Rosaria R Papulino Chiara C Sgueglia Giulia G Chianese Ugo U De Marchi Tommaso T Iovino Francesco F Rotili Dante D Mai Antonello A Niméus Emma E Dell' Aversana Carmela C Altucci Lucia L

Cancers 20210201 3

The efficacy and side effects of endocrine therapy in breast cancer (BC) depend largely on estrogen receptor alpha (ERα) expression, the specific drug administered, and treatment scheduling. Although the benefits of endocrine therapy outweigh any adverse effects in the initial stages of BC, later- or advanced-stage tumors acquire resistance to treatments. The mechanisms underlying tumor resistance to therapy are still not well understood, posing a major challenge for BC patient care. Epigenetic ...[more]

PMID: 33535487

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Characterization of AR interactome in prostate cancer cells after MC3324 treatment

Project description:We here investigated the alterations in the androgen receptor (AR) itneractome after treatment with the dual-KDM inhibitor MC3324.

2022-10-13 | PXD029249 | Pride

Murine C2C12 cells: GTP-stimulated cells vs. Control in SM

Project description:To define the signalling of extracellular GTP as enhancer of myogenesis, we investigated if the gene expression profile of differentiated C2C12 cells (4 and 24 hours in SM) was affected by extracellular GTP. Two-condition experiment, GTP-treated C2C12 cells vs Control C2C12 cells at 4 h and 24 h of differentiation. Biological replicates: 1 control, 1 GTP-treated cells, independently grown and harvested. One replicate per array.

2010-06-20 | E-GEOD-18531 | biostudies-arrayexpress

Characterization of the roles of the RNA-binding protein AUF-1 in airway epithelial inflammatory responses

Project description:The RNA-binding protein AU-rich-element factor-1 (AUF-1) regulates mRNA decay and translation of genes during inflammation and cellular senescence, two pathogenic mechanisms of chronic obstructive pulmonary disease (COPD). Decreased AUF-1 expression was described in bronchiolar epithelium of COPD patients versus controls and in vitro cytokine-challenged airway epithelial cells, prompting the identification of epithelial AUF-1-targeted transcripts and function. RNA immunoprecipitation-sequencing (RIP-Seq) identified, in the human BEAS-2B cell line, 494 AUF-1-bound mRNAs enriched in their 3’-untranslated regions for a Guanine-Cytosine (GC)-rich binding motif, selectively confirmed by biotin pulldown. AUF-1-targets’ steady-state levels were equally affected by partial or near-total AUF-1 loss induced by cytomix (TNF/IL1/IFN/10 nM each) and siRNA, respectively, with differential transcript decay rates. Cytomix-decreased AUF-1 levels in BEAS-2B and primary human small-airways epithelium (HSAEC) associated with cell-cycle arrest, increased lysosomal damage and senescence-associated secretory phenotype (SASP) factors and with increased AUF-1 in extracellular vesicles. In-silico analysis found enriched AUF-1-targets in COPD-related pathways, SASP proteome atlas, transcriptomic COPD databases of HSAEC, lung tissue and single-cell RNA-sequencing. Intracellular and exosomal-associated AUF-1 may mediate airway epithelial inflammatory responses.

2023-04-14 | E-MTAB-12583 | biostudies-arrayexpress

Ruminococcus torques is a keystone degrader of intestinal mucin glycoprotein, releasing oligosaccharides used by Bacteroides thetaiotaomicron

Project description:Symbiotic interactions between humans and our communities of resident gut microbes (microbiota) play many roles in health and disease. Some gut bacteria utilize mucus as a nutrient source and can under certain conditions damage the protective barrier it forms, increasing disease susceptibility. We investigated how Ruminococcus torques—a known mucin-degrader that remains poorly studied despite its implication in inflammatory bowel diseases (IBDs)— degrades mucin glycoproteins or their component O-linked glycans to understand its effects on the availability of mucin-derived nutrients for other bacteria. We found that R. torques utilizes both mucin glycoproteins and released oligosaccharides from gastric and colonic mucins, degrading these substrates with a panoply of mostly constitutively expressed, secreted enzymes. Investigation of mucin oligosaccharide degradation by R. torques revealed strong fucosidase, sialidase and 1,4-galactosidase activities. There was a lack of detectable sulfatase and weak β1,3-galactosidase degradation, resulting in accumulation of glycans containing these structures on mucin polypeptides. While the Gram-negative symbiont, Bacteroides thetaiotaomicron grows poorly on mucin glycoproteins, we demonstrate a clear ability of R. torques to liberate products from mucins, making them accessible to B. thetaiotaomicron. This work underscores the diversity of mucin-degrading mechanisms in different bacterial species and the probability that some species are contingent on others for the ability to more fully access mucin-derived nutrients. The ability of R. torques to directly degrade a variety of mucin and mucin glycan structures and unlock released glycans for other species suggests that it is a keystone mucin degrader, which may contribute to its association with IBD.

2024-06-19 | PXD051107 | Pride

Assessing actin-pathway interactions in variants identified in patients with ocular coloboma

Project description:We used whole exome sequence to identify de novo mutations in patients with ocular coloboma. Three of these encoded actin pathway components, ACTG1, TWF1 and LCP1. Mass spectrometry-based interactomes of wild-type and mutant proteins were performed to reveal altered functional interactions for all three variants.

2017-05-24 | PXD005090 | Pride

Murine C2C12 cells: GTP-stimulated cells vs. Control in DM

Project description:To define the signalling of extracellular GTP as enhancer of myogenesis, we investigated if the gene expression profile of differentiated C2C12 cells (4 hours in DM) was affected by extracellular GTP. Two-condition experiment, GTP-treated C2C12 cells vs Control C2C12 cells at 4 h of differentiation. Biological replicates: 1 control, 1 GTP-treated cells, independently grown and harvested. One replicate per array.

2010-06-20 | E-GEOD-18584 | biostudies-arrayexpress

Protein arginine methyltransferase 5 (PRMT5) is an actionable therapeutic target in CDK4/6 inhibitor-resistant ER+/RB-deficient breast cancer

Project description:PRMT5 Co-IP mass spectrometry: Lysates of MCF-7 RB1-knockout cells were pulled down with a PRMT5 antibody or IgG control. The pulldowns were subjected to mass spectrometry analysis. QEX2_981005, QEX2_981006, QEX2_981007: DMSO, IgG QEX2_981008, QEX2_981009, QEX2_981010: DMSO, PRMT5 antibody QEX2_981011, QEX2_981012, QEX2_981013, GSK, IgG QEX2_981014, QEX2_981015, QEX2_981016, GSK, PRMT5 antibody SDMA PTM analysis: MCF-7 RB1-knockout cells were transfected with a PRMT5 siRNA or a control siRNA. Lysates were collected three days after transfection and subjected to mass spectrometry analysis. LUM1_1000791, LUM1_1000792, LUM1_1000793: control SiRNA LUM1_1000794, LUM1_1000795, LUM1_1000796: PRMT5 siRNA [

2024-01-12 | PXD046996 | Pride

The Plant Unique ESCRT Component FREE1 Regulates Autophagosome Closure

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2023-03-30 | PXD040435 | Pride

Chd1 regulates repair of promoter-proximal DNA breaks to sustain hypertranscription in embryonic stem cells

Project description:Stem and progenitor cells undergo a global elevation of nascent transcription, or hypertranscription, during key developmental transitions involving rapid cell proliferation. The chromatin remodeler Chd1 binds to RNA Pol I and II genes and is required for hypertranscription in embryonic stem (ES) cells in vitro and the early post-implantation epiblast in vivo. Biochemically, Chd1 has been shown to facilitate transcription at least in part by removing nucleosomal barriers to elongation, but its mechanism of action in stem cells remains poorly understood. Here we report a novel role for Chd1 in the repair of promoter-proximal endogenous double-stranded DNA breaks (DSBs) in ES cells. An unbiased proteomics approach revealed that Chd1 interacts with several DNA repair factors including ATM, Parp1, Kap1 and Topoisomerase 2. We show that wild-type ES cells display high levels of phosphorylated H2AX and Kap1 at chromatin, notably at rDNA in the nucleolus, in a Chd1-dependent manner. Loss of Chd1 leads to an extensive accumulation of DSBs at Chd1 target Pol II genes and rDNA. Genes prone to DNA breaks in Chd1-null ES cells tend to be longer genes with GC-rich promoters, a more labile nucleosomal structure and roles in chromatin organization, transcription and signaling. These results reveal a vulnerability of hypertranscribing stem cells to endogenous DNA breaks, with important implications for developmental and cancer biology.

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A balanced Oct4 protein interaction network is crucial for maintaining pluripotency

Project description:Oct4 is considered a master transcription factor for pluripotent cell self-renewal and embryo development. It primarily collaborates with other transcriptional factors or coregulators to maintain pluripotency. However, it is still unclear how Oct4 interacts with its partners. Here, we show that the Oct4 linker interface mediates competing and balanced Oct4 protein interactions which are crucial for maintaining pluripotency. Linker mutant ESCs maintain the key pluripotency genes expression, but show decreased expression of self-renewal genes and increased expression of differentiation genes which result in impaired ESCs self-renewal and early embryonic lethality. Linker mutation dose not affect Oct4 genomic binding and transactivation potential, but breaks the balanced Oct4 interactome. In mutant ESCs, the interaction between Oct4 and Klf5 was decreased, but interactions between Oct4 and Cbx1, Ctr9, Cdc73 were increased which disrupt the epigenetic state of ESCs. Overexpression of Klf5 or knockdown Cbx1, Cdc73 rescue the cellular phenotype of linker mutant ESCs by rebalancing Oct4 interactome indicating that different partners interact with Oct4 competitively. Thus, by showing how Oct4 interacts with different partners, we provide novel molecular insights to explain how Oct4 contributes to the maintenance of pluripotency.

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