Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tubulin Tyrosine Ligase Like 4 (TTLL4) overexpression in breast cancer cells alters exosome biogenesis and promotes brain metastasis

ABSTRACT: The survival rate is poor in breast cancer patients with brain metastases. Thus, new concepts for therapeutic approaches are required. During metastasis, the cytoskeleton of cancer cells is highly dynamic and therefore cytoskeleton-associated proteins are interesting targets for tumour therapy.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Breast Cancer

SUBMITTER: Christoph Krisp

LAB HEAD: Sabine Windhorst

PROVIDER: PXD020743 | Pride | 2021-08-20

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Publications

Tubulin Tyrosine Ligase Like 4 (TTLL4) overexpression in breast cancer cells is associated with brain metastasis and alters exosome biogenesis.

Arnold Julia J Schattschneider Juliana J Blechner Christine C Krisp Christoph C Schlüter Hartmut H Schweizer Michaela M Nalaskowski Marcus M Oliveira-Ferrer Leticia L Windhorst Sabine S

Journal of experimental & clinical cancer research : CR 20200930 1

<h4>Background</h4>The survival rate is poor in breast cancer patients with brain metastases. Thus, new concepts for therapeutic approaches are required. During metastasis, the cytoskeleton of cancer cells is highly dynamic and therefore cytoskeleton-associated proteins are interesting targets for tumour therapy.<h4>Methods</h4>Screening for genes showing a significant correlation with brain metastasis formation was performed based on microarray data from breast cancer patients with long-term fo ...[more]

PMID: 32998758

Similar Datasets

Identification of Bona Fide Targets of AMPylating Fic-enzymes by Substrate Mediated Covalent Capture

Project description:Many pathogenic bacteria utilize posttranslational modifications to manipulate central components of the host cell functions. Often, the released enzymes belong to the large Fic-family, causing target modification with nucleotide monophosphates. Due to the lack of a generic method for the identification of the Fic-family’s cellular targets, we have established a new approach by combining synthetic thiol-reactive nucleotide derivatives (TReNDs) with recombinantly produced Fic-enzymes containing strategically placed cysteines in their active sites, thereby producing reactive binary FicTReND probes for covalent substrate capture. The binary probes successfully capture their targets from complex lysates and permit their identification by mass spectrometry.

2020-07-09 | PXD015599 | Pride

Proteomics of lung tissues from COVID19 patients

Project description:Coagulopathy is a hallmark finding in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is associated with an increased risk of death from venous and arterial thromboembolic complications. SARS-CoV-2 infection can lead to microvascular thrombosis that contributes to acute lung injury and respiratory failure. The molecular mechanisms leading to thrombosis in Coronavirus disease 2019 (COVID19) patients are poorly understood. Here, we study a role of the procoagulant neutrophil extracellular traps (NETs)/Factor XII (FXII) axis in COVID19-associated thromboembolism.

2021-08-20 | PXD020216 | Pride

Characterization of exosomes from highly metastatic pancreatic adenocarcinoma line: ASML and a CD44v kd of ASML based on their miRNA content

Project description:Comparing the miRNA profile of exosomes from ASML vs ASML CD44v kd pancreatic adenocarcinoma line revealed that the expression level of 33 from the 40 most abundant miRNA differed significantly between ASMLwt and ASML-CD44vkd exosomes In this study tumor cell exosomes, deemed important for intercellular communication were analysed for their miRNA content. Exosomes from a highly metastatic pancreatic adenocarcinoma cell line, ASML and from a CD44v kd of ASML were used for RNA preparation using Trizol reagent, and the total RNA was sent to Genomics core facility,EMBL, Heidelberg for miRCURY LNA microRNA Array, v.11.0 - hsa, mmu & rno

2011-12-28 | E-GEOD-34738 | biostudies-arrayexpress

Cardiotoxicity of tubulin binders

Project description:The use of tubulin binders (TBs) in oncology indications often is associated with cardiotoxicity, the mechanism of which has not been elucidated. We observed that a single administration of TBs to rats caused an increase in the number of mitotic figures in the myocardial interstitium after 24 hours. We therefore hypothesized that interstitial cells are the primary target of TBs. To test this hypothesis, we evaluated the acute effects of a single intravenous administration of 3 reference TBs, colchicine (0.2 and 2 mg/kg), vinblastine (0.5 and 3 mg/kg), and vincristine (0.1 and 1 mg/kg) 6 and 24 hours after dosing. Mitotic arrest was identified at 24 hours in all high-dose groups based on an increase in the number of mitotic figures in the interstitium coupled with a dramatic decrease in the number of Ki67-positive interstitial cells. Analysis of the myocardial transcriptomic data further supported G2/M cell cycle arrest 6 hours after dosing with the high-dose groups of all 3 compounds. Apoptotic figures and an increase in the number of cleaved caspase 3-positive cells were identified at 6 and 24 hours at the highest dose of each compound almost exclusively in interstitial cells; a few cardiomyocytes were affected as well. Transcriptomic data further suggested that some of the affected interstitial cells were endothelial cells based on the up-regulation of genes typically associated with vascular damage and down-regulation of Endothelial Cell-Specific Molecule 1 and Apelin. Taken together, these data identify endothelial cells of the myocardium as the primary target of the cardiotoxicity of TBs and identify cell cycle arrest as the mechanism of this toxicity. Gene expression was profiled in the myocardium of rats at 6 and 24 hr after a single dose of colchicine, vinblastine or vincristine.

2010-01-01 | E-GEOD-19290 | biostudies-arrayexpress

Exosomal tumor miRNA modulates premetastatic organ cells

Project description:This SuperSeries is composed of the following subset Series: GSE34737: Comparative analysis of mRNA expression in untreated lymph node stroma cells and upon treatment with exosomes derived from ASMLwt, ASML cd44v knockdown cells. GSE34738: Characterization of exosomes from highly metastatic pancreatic adenocarcinoma line: ASML and a CD44v kd of ASML based on their miRNA content Refer to individual Series

2011-12-28 | E-GEOD-34739 | biostudies-arrayexpress

Transcriptional profiling of early differentiation of primary human mesenchymal stem cells into chondrocytes

Project description:Transcriptional profiling of undifferentiated MSCs, MSCs in 3D culture, early differentiation time-points 15m, 30m, 1h, 2h, 4h, 8h, 16h after induction with TGF-β3 and hyaluronic acid, and fully differentiated chondrocytes (21 days after induction) using RNA-seq in triplicates of clones.

2021-05-24 | E-MTAB-10476 | biostudies-arrayexpress

Gene expression profiling of WWOX-overexpressing glioblastoma T98G cells

Project description:The WWOX gene is known for its tumor suppressor character and seems to be one of the main cellular regulators of cell cycle and apoptosis. The aim of the study was to identify cellular pathways and biological processes influenced by WWOX in glioblastoma cells. Our experiment showed that in this type of cancer WWOX, beside cell cycle and apoptosis control, may be involved in metabolism, cytoskeleton structure and differentiation. T98G glioblastoma cells were stably transfected with WWOX cDNA. T98G cells transfected with an empty vector served as a control. Total mRNA was isolated to look for gene-expression differences induced by the WWOX overexpression.

2013-10-22 | E-GEOD-51481 | biostudies-arrayexpress

Age-dependent RGS5 loss in pericytes induces cardiac dysfunction and fibrosis in the heart

Project description:Background. Ageing is one of the main risk factors of cardiovascular disease. Pericytes are capillary-associated mural cells involved in the maintenance and stability of the vascular network. In the heart, the consequences of ageing on cardiac pericytes are unknown. Methods. In this study, we have combined single nucleus RNA sequencing and histological analysis to determine the effects of ageing on cardiac pericytes. Furthermore, we have conducted in vivo and in vitro analysis of RGS5 loss of function and finally have perfomed pericytes-fibroblasts co-culture studies to understand the effect of RGS5 loss of function in pericytes on the neighbouring fibroblasts. Results. We showed that ageing reduces the pericyte area and coverage. Single nucleus RNA sequencing analysis further revealed that the expression of the Regulator of G protein signalling 5 (Rgs5) is reduced in old cardiac pericytes. In vivo and in vitro studies showed that the deletion of RGS5 induces morphological changes and a pro-fibrotic gene expression signature characterized by the expression of different extracellular matrix components and growth factors like TGFB2 and PDGFB in pericytes. Indeed, the culture of fibroblasts with the supernatant of RGS5 deficient pericytes induced their activation characterized by the increased expression of α smooth muscle actin in a TFGβ2 dependent mechanism. Conclusions. Our results identify RGS5 as a crucial regulator of pericyte function during cardiac ageing. The deletion of RGS5 causes cardiac dysfunction and induces myocardial fibrosis, one of the hallmarks of cardiac ageing.

2024-03-06 | E-MTAB-13841 | biostudies-arrayexpress

Transcription profiling by array of human dendritic cells exposed to mesenchymal stem cells

Project description:All experiments are performed on human dendritic cells (DCs) differentiated in GM-CSF and IL-4 from CD14+ cells and bone marrow mesenchimal stem cells (MSCs). We found that MSCs impair active immune synapse formation and we evidenced at electron microscopy two types of contact between MSCs and DCs: gap and adherent junctions. In the same experiments we show that MSC contacts induce a reorganization of DC cytoskeleton by the formation of actin podosomes, structures typical of an immature, tolerogenic state of DCs. These results suggest that MSCs exert a tolerogenic effect on DCs by mechanism mediated by cell-cell contact. This induces DC cytoskeleton reorganization with formation of actin podosomes.

2010-12-31 | E-MTAB-286 | biostudies-arrayexpress

Neuroserpin Is Strongly Expressed in the Developing and Adult Mouse Neocortex but Its Absence Does Not Perturb Cortical Lamination and Synaptic Proteome

Project description:Neuroserpin is a serine protease inhibitor that regulates the activity of tissue-type plasminogen activator (tPA) in the nervous system. Neuroserpin is strongly expressed during nervous system development as well as during adulthood, when it is predominantly found in regions eliciting synaptic plasticity. In the hippocampus, neuroserpin regulates developmental neurogenesis, synaptic maturation and in adult mice it modulates synaptic plasticity and controls cognitive and social behavior. High expression levels of neuroserpin in the cerebral cortex starting from prenatal stage and persisting during adulthood suggest an important role for the serpin in the formation of this brain region and in the maintenance of cortical functions. In order to uncover neuroserpin function in the cerebral cortex, in this work we performed a comprehensive investigation of its expression pattern during development and in the adulthood. Moreover, we assessed the role of neuroserpin in cortex formation by comparing cortical lamination and neuronal maturation between neuroserpin-deficient and control mice. Finally, we evaluated a possible regulatory role of neuroserpin at cortical synapses in neuroserpin-deficient mice. We observed that neuroserpin is expressed starting from the beginning of corticogenesis until adulthood throughout the cortex in both glutamatergic projection neurons and GABA-ergic interneurons. However, in the absence of neuroserpin we did not detect any alteration in cortical layer formation, in soma size, in dendritic length, and the ultrastructure. Furthermore no significant quantitative changes could be observed in the proteome of cortical synapses could be observed upon Neuroserpin deficiency. We conclude that, although strongly expressed in the cerebral cortex, absence of neuroserpin does not lead to developmental abnormalities, and does not perturb composition of the cortical synaptic proteome.

2021-02-23 | PXD022371 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data