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Consequences of Cyp2c44 deletion on proteome of the microsomal fraction of primary polyoma middle T (PyMT) tumors

ABSTRACT: Here we compared the proteomes of microsomal fractions from primary tumors isolated from PyMT mice versus PyMTxCyp2c44-/- mice.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Primary Cell

SUBMITTER: Ilka Wittig

LAB HEAD: Ingrid Fleming

PROVIDER: PXD017303 | Pride | 2020-03-03

REPOSITORIES: Pride

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			Action	DRS
	150930_RK_isoformes_10_01.raw	Raw
	150930_RK_isoformes_10_02.raw	Raw
	150930_RK_isoformes_10_03.raw	Raw
	150930_RK_isoformes_10_04.raw	Raw
	150930_RK_isoformes_1_01.raw	Raw

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Publications

Cyp2c44 regulates prostaglandin synthesis, lymphangiogenesis, and metastasis in a mouse model of breast cancer.

Kesavan Rushendhiran R Frömel Timo T Zukunft Sven S Laban Hebatullah H Geyer Alexandra A Naeem Zumer Z Heidler Juliana J Wittig Ilka I Elwakeel Eiman E Brüne Bernhard B Weigert Andreas A Popp Rüdiger R Fleming Ingrid I

Proceedings of the National Academy of Sciences of the United States of America 20200302 11

Arachidonic acid epoxides generated by cytochrome P450 (CYP) enzymes have been linked to increased tumor growth and metastasis, largely on the basis of overexpression studies and the application of exogenous epoxides. Here we studied tumor growth and metastasis in Cyp2c44<sup>-/-</sup> mice crossed onto the polyoma middle T oncogene (PyMT) background. The resulting PyMT<sup>2c44</sup> mice developed more primary tumors earlier than PyMT mice, with increased lymph and lung metastasis. Primary tum ...[more]

PMID: 32123095

Similar Datasets

Consequences of Cyp2c44 deletion in the polyoma middle T (PyMT) breast cancer tumor proteome

Project description:Comparison of the proteome of intact primary breast cancer tumors from PyMT mice versus PyMTxCyp2c44-/- mice.

2020-03-03 | PXD017336 | Pride

Consequences of sEH deletion in the polyoma middle T (PyMT) breast cancer tumor proteome

Project description:The aim of this investigation was to study the consequences of interfering with soluble epoxide hydrolase (sEH) expression on tumor growth and metastasis in genetically modified animals that spontaneously generate tumors without the exogenous application of high concentrations of epoxide mediators or inhibitors. Therefore, breast cancer development was studied in mice expressing the polyoma middle T oncogene (PyMT) under the control of the mouse mammary tumor virus promoter, to induce spontaneous mammary tumors. To facilitate the study of endogenous sEH activity in tumor growth, PyMT mice were then crossed with sEH-/- mice to generate sEH-deficient mice that spontaneously generate breast tumors (so called PyMTsEH mice). For these analyses, primary tumors were removed from 20 week old mice.

2021-09-14 | PXD026214 | Pride

A microsomal proteomics view of H2O2- and ABA-dependent responses

Project description:The plant hormone abscisic acid (ABA) modulates a number of plant developmental processes and responses to stress. In planta, ABA has been shown to induce reactive oxygen species (ROS) production through the action of plasma membrane-associated NADPH oxidases. Although quantitative proteomics studies have been performed to identify ABA- or hydrogen peroxide (H2O2)-dependent proteins, little is known about the ABA- and H2O2-dependent microsomal proteome changes. Here, we examined the effect of 50 µM of either H2O2 or ABA on the Arabidopsis microsomal proteome using tandem mass spectrometry and identified 86 specifically H2O2-dependent and 52 specifically ABA-dependent proteins that are differentially expressed. We observed differential accumulation of proteins involved in the TCA cycle notably in response to H2O2. Of these, aconitase 3 responded to both H2O2 and ABA. Additionally, over 30 proteins linked to RNA biology responded significantly to both treatments. Gene ontology categories such as ‘response to stress’ and ‘transport’ were enriched, suggesting that H2O2 or ABA directly and/or indirectly cause complex and partly overlapping cellular responses.

2017-08-22 | PXD006513 | Pride

Complexome profiling of human cybrids laking mitochondrial genes Cox1 or Cox2

Project description:Mitochondrial respiratory chain (MRC) complexes I, III and IV are associated into large molecular structures named supercomplexes (SCs) or respirasomes, whose functional roles remain to be fully understood. Biochemical analyses in a diversity of OXPHOS-deficient cellular and animal models support the idea that one of the SCs function is to confer stability to individual MRC complexes, in particular to complex I (CI). To gain insight into the mechanisms that regulate the structural interdependences among MRC complexes, we performed complexome profiling of human cybrids laking mitochondrial genes Cox1 or Cox2 and compared protein assemblies and intermediates to control 143B cells.

2020-07-01 | PXD017840 | Pride

Identification of NOS3 interacting proteins

Project description:The endothelial nitric oxide (NO) synthase (eNOS, or NOS3) can be activated in response to fluid shear stress and numerous agonists via cellular events such as increased intracellular Ca2+, interaction with substrate, co-factors as well as adaptor and regulatory proteins, protein phosphorylation and S-glutathionylation in addition to shuttling between distinct sub-cellular domains. While some protein interactors modulate enzymatic activity, others can be S-nitrosation targets, which are brought in close proximity to the NO source under specific conditions. The identification of proteins interacting with eNOS in human endothelial cells stimulated with serum and growth factors may provide new insight into the regulation of eNOS activity as well as NO signaling via S-nitrosation.

2021-09-08 | PXD013755 | Pride

Quantitative LC-MS/MS Proteomics of microsomal fractions from adult human livers

Project description:We report label-free and targeted quantification of xenobiotic metabolizing enzymes (XME) and transporters in 39 human liver microsomal samples. More than 2800 proteins were identified and quantified. These data can be used in physiologically based pharmacokinetic models for dosage regimen design and precision dosing.

2021-09-09 | PXD021025 | Pride

Regulation of the microsomal proteome by salicylic acid and deficiency of phosphatidylinositol‐4‐kinases β1 and β2 in Arabidopsis thaliana

Project description:Phosphatidylinositol-4-kinases β1 and β2 (PI4Kβ1/PI4Kβ2), which are responsible for phosphorylation of phosphoinositol to phosphatidylinositol-4-phosphate, have an important role in vesicular trafficking in plants. Moreover, PI4Kβ1/PI4β2 negatively regulate biosynthesis of phytohormone salicylic acid (SA). SA plays crucial role in plant immune responses and its endogenous concentration strongly affects plant transcriptome. In this study we were focused on the effect of the PI4Kβ1/PI4Kβ2 and SA on the abundance of membrane proteins. For this purpose, we performed proteomic analysis on isolated microsomal fractions from leaves of four Arabidopsis thaliana genotypes: wild type ecotype Columbia-0; double mutant impaired in function of PI4Kβ1/PI4Kβ2 (pi4kβ1/pi4kβ2) exhibiting high SA level; sid2 mutant with impaired SA biosynthesis depending on the isochorismate synthase 1 and triple mutant sid2/pi4kβ1/pi4kβ2. In total, we identified 4534 proteins from which 1696 proteins differed in abundance between the mutants and WT. We showed that SA has a big impact on membrane proteome, because among hundreds of the identified affected proteins typical proteins associated with SA triggered pathway occurred. Our data thus point out new connections between SA pathway and clathrin independent endocytosis (flotillins) and exocytosis/protein secretion (syntaxins, tertraspanin) to be investigated in future. In contrast to SA, presence/absence of PI4Kβ1/PI4Kβ2 itself affected only 27 proteins. Nevertheless, among them we identified CERK1, plasma membrane receptor for chitin. Although PI4Kβ1/PI4Kβ2 itself did not have strong impact on A. thaliana microsomal proteome, our data clearly shows that PI4Kβ1/PI4Kβ2 enhance the proteome changes when SA pathway is modulated in parallel

2021-02-24 | PXD019737 | Pride

Sulfenylation of Human Liver and Kidney Microsomal Cytochromes P450 and Other Drug Metaboing Enzymes as a Response to Redox Alteration

Project description:The lumen of the endoplasmic reticulum (ER) provides an oxidizing environment to aid in the formation of disulfide bonds, which is tightly regulated by both antioxidant proteins and small molecules. On the cytoplasmic side of the ER, cytochrome P450 (P450) proteins have been identified as a superfamily of enzymes that are important in the formation of endogenous chemicals as well as in the detoxication of xenobiotics. Our previous report described oxidative inhibition of P450 Family 4 enzymes via oxidation of the heme-thiolate cysteine to a sulfenic acid (-SOH) (Albertolle, M. E. et al. (2017) J. Biol. Chem. 292, 11230-11242). Further proteomic analyses of murine kidney and liver microsomes led to the finding that a number of other drug metabolizing enzymes located in the ER are also redox-regulated in this manner. We expanded our analysis of sulfenylated enzymes to human liver and kidney microsomes. Evaluation of the sulfenylation, catalytic activity, and spectral properties of P450s 1A2, 2C8, 2D6, and 3A4 led to the identification of two classes of redox sensitivity in P450 enzymes: heme thiolate-sensitive and thiol-insensitive. These findings provide evidence for a mammalian P450 regulatory mechanism, which may also be relevant to other drug-metabolizing enzymes.

2018-01-29 | PXD007913 | Pride

The Daphnia cuticle proteome - whole cuticle samples

Project description:The cuticles of arthropods, including aquatic crustaceans like Daphnia, provide an interface between the organism and its environment. Thus, the cuticle’s structure influences how the organism responds to and interacts with its surroundings. Here, we used label-free quantification proteomics to provide a proteome of the molted cuticle of Daphnia magna, which has long been a prominent subject of studies on ecology, evolution, and developmental biology, anddetected 278 high confidence proteins. Using protein sequence domain and functional enrichment analyses, we identified chitin-binding structural proteins and chitin modifying enzymes as most abundant protein groups in the cuticle proteome.Structural cuticular protein families showed a similar distribution to those found in other arthropods and indicated proteins responsible for the soft and flexible structure of the Daphnia cuticle . Finally, cuticle protein genes were clustered as tandem gene arrays in the Daphnia genome, indicating their importance for adaptation to environmental change. The cuticle proteome presented here will be a valuable resource to the Daphnia research community, informing investigations on diverse topics such as the genetic basis of interactions with predators and parasites.

2024-09-02 | PXD040228 | Pride

Apc mutation enhances PyMT-induced mammary tumorigenesis.

Project description:The Adenomatous Polyposis Coli (APC) tumor suppressor gene is silenced by hypermethylation or mutated in up to 70% of human breast cancers. In mouse models, Apc mutation disrupts normal mammary development and predisposes to mammary tumor formation; however, the cooperation between APC and other mutations in breast tumorigenesis has not been studied. To test the hypothesis that loss of one copy of APC promotes oncogene-mediated mammary tumorigenesis, Apc(Min/+) mice were crossed with the mouse mammary tumor virus (MMTV)-Polyoma virus middle T antigen (PyMT) or MMTV-c-Neu transgenic mice. In the PyMT tumor model, the Apc(Min/+) mutation significantly decreased survival and tumor latency, promoted a squamous adenocarcinoma phenotype, and enhanced tumor cell proliferation. In tumor-derived cell lines, the proliferative advantage was a result of increased FAK, Src and JNK signaling. These effects were specific to the PyMT model, as no changes were observed in MMTV-c-Neu mice carrying the Apc(Min/+) mutation. Our data indicate that heterozygosity of Apc enhances tumor development in an oncogene-specific manner, providing evidence that APC-dependent pathways may be valuable therapeutic targets in breast cancer. Moreover, these preclinical model systems offer a platform for dissection of the molecular mechanisms by which APC mutation enhances breast carcinogenesis, such as altered FAK/Src/JNK signaling.

| S-EPMC3245255 | biostudies-literature

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