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RNAseq analysis of integrin β3-mediated responses to in vitro docetaxel in PyMT-BO1 breast cancer cells

ABSTRACT: We sought to transcriptomically characterize the effect of integrin β3 expression on breast cancer cell responses to the microtubule-inhibiting chemotherapeutic agent docetaxel. Experiments were performed in PyMT-BO1 murine breast cancer cells with CRISPR mediated deletion of the Itgb3 gene. Cells were subsequently retrovirally rescued using either an empty vector construct (pMx), a functional human integrin β3 construct (hβ3), or a signaling-deficient integrin β3 mutant.

ORGANISM(S): Mus musculus

PROVIDER: GSE166315 | GEO | 2021/02/08

REPOSITORIES: GEO

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RNAseq analysis of integrin β3-mediated responses to in vitro docetaxel in 4T1 breast cancer cells

Project description:We sought to transcriptomically characterize the effect of integrin β3 expression on breast cancer cell responses to the microtubule-inhibiting chemotherapeutic agent docetaxel. Experiments were performed in 4T1 murine breast cancer cells with or without CRISPR mediated deletion of the Itgb3 gene.

2021-02-11 | GSE166536 | GEO

IGDQ motogenic peptide gradient induces directional cell migration through integrin (αv)β3 activation in metastatic breast cancer

Project description:In the context of breast cancer metastasis study, we have shown in an in vitro model of cell migration that IGDQ-exposing (IsoLeu-Gly-Asp-Glutamine type I Fibronectin motif) monolayers (SAMs) on gold sustain the adhesion of MDA-MB-231 cells by triggering Focal Adhesion Kinase by activating integrins. Such tunable scaffolds are used to mimic the extracellular environment, inducing and controlling cell migration towards an anisotropic surface. The observed migratory behavior induced by the IGDQ-bearing peptide gradient along the surface suggests the presence of cell subpopulations: “stationary” or a “migratory” phenotype. We focused on the integrins α5(β1) and (αv)β3, already known to be implicated in cell migration. To this aim, a whole proteomic analysis was performed in beta 3 integrin (ITGB3) or alpha 5 integrin (ITGA5) knock-down MDA-MB-231, in order to highlight the pathways implied into the integrin-dependent cell migration. Our results showed that i) ITGB3 depletion influenced ITGA5 mRNA expression, ii) ITGB3 and ITGA5 were both necessary for IGDQ-mediated directional single cell migration, iii) integrin (αv)β3 was activated by IGDQ fibronectin type I motif and iv) co-regulation of retrograde transport of ITGB3 by ITGA5 is potentially necessary for directional IGDQ-mediated cell migration.

2022-11-08 | PXD024540 | Pride

RNAseq analysis of integrin β3-mediated responses to in vitro docetaxel in 4T1 breast cancer cells

Project description:RNAseq analysis of integrin β3-mediated responses to in vitro docetaxel in 4T1 breast cancer cells

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RNAseq analysis of integrin β3-mediated responses to in vitro docetaxel in PyMT-BO1 breast cancer cells

Project description:RNAseq analysis of integrin β3-mediated responses to in vitro docetaxel in PyMT-BO1 breast cancer cells

| PRJNA700430 | ENA

Cancer burden is controlled by mural cell- β3-integrin regulated crosstalk with tumor cells

Project description:Phosphoproteomics analysis were performed in WT and β3-integrin-null pericytes. On the other hand, phosphoproteomics experiments were done in B16F0 melanoma cells treated for 24 hours with conditioned medium from WT and β3-integrin-null pericytes.

2020-06-01 | PXD014513 | Pride

The Itgb3 Adhesome - Integrin β3 is seen as a key anti-angiogenic target for cancer treatment due to its expression on neovasculature

Project description:Integrin β3 is seen as a key anti-angiogenic target for cancer treatment due to its expression on neovasculature, but the role it plays in the process is complex; whether it is pro- or anti-angiogenic depends on the context in which it is expressed. To understand precisely β3’s role in regulating integrin adhesion complexes in endothelial cells, we characterised, by mass spectrometry, the β3-dependent adhesome. We show that depletion of β3-integrin in this cell type leads to changes in microtubule behaviour that control their migration. β3-integrin regulates microtubule stability in endothelial cells through Rcc2/Anxa2 driven control of active Rac1 localisation. Our findings reveal that angiogenic processes, both in vitro and in vivo, are more sensitive to microtubule targeting agents when β3-integrin levels are reduced.

2018-05-23 | PXD008591 | Pride

Integrin beta 3 regulates cellular senescence by activating the TGFβ pathway

Project description:Cellular senescence is an important in vivo mechanism that prevents the propagation of damaged cells. However, the precise mechanism(s) regulating senescence are not well characterized. Here, we find that ITGB3 (integrin beta 3 or β3) is epigenetically regulated by the Polycomb protein CBX7. β3 expression accelerates the onset of senescence in human primary fibroblasts, by activating the TGFβ pathway in a cell autonomous and non-cell autonomous manner. β3 levels are dynamically increased during oncogeneinduced senescence (OIS) through CBX7 epigenetic regulation. DNA-damage and therapy-induced senescence (TIS) also induce β3 expression. In fact, downregulation of β3 levels override OIS and TIS, independently of its ligand-binding activity. Moreover, cilengitide, a αvβ3 antagonist, has the ability to block the SASP without affecting proliferation. Finally, we show an increase in β3 levels during aging in mice and humans. Altogether, our data show that integrin β3 subunit is a marker and regulator of senescence.

2017-03-09 | PXD005717 | Pride

Connecting extracellular vesicle uptake and exosome biogenesis: intercellular communication in breast cancer cells is ITGB3-dependent

Project description:Metastasis, the spread of malignant cells from the primary tumour to distant sites is in 90% of the cases, the ultimate cause cancer related death. The integrin ITGB3 has been previously described to play an essential role in breast cancer metastasis, but the precise mechanisms remain undefined. We have now uncovered essential and thus far unknown roles of ITGB3 in vesicle uptake and exosome biogenesis. The functional requirement on ITGB3 is founded in its described interactions with heparan sulphated glyco-proteins (HSPGs) and the process of integrin recycling, allowing the capture of extracellular vesicles and their endocytosis-mediated internalisation. Key for the function of ITGB3 is the interaction and activation of the focal adhesion kinase (FAK), which is required for endocytosis of this vesicles and the entry of the endocytosis derived early endosomes into the exosome biogenesis pathway. Thus, ITGB3 has a central role in intracellular communication via extracellular vesicles, proposed to be critical for cancer metastasis.

2020-07-14 | PXD013489 | Pride

In Vivo RNA Interference Screening Identifies a Leukemia-Specific Dependence on Integrin Beta 3 Signaling

Project description:Primary leukemia stem cells (LSCs) reside in an in vivo microenvironment that supports the growth and survival of malignant cells. We used an in vivo short hairpin RNA (shRNA) screening approach to identify novel genes that are essential for primary murine MLL-AF9 acute myeloid leukemia (AML). We found that Integrin Beta 3 (Itgb3) is selectively essential for murine leukemia cells in vivo, and for human leukemia cells in xenotransplantation studies. In leukemia cells, Itgb3 knockdown impaired homing, downregulated LSC transcriptional programs, and induced differentiation. In contrast, loss of Itgb3 in normal HSPCs did not affect engraftment, reconstitution, or differentiation in long term transplantation assays. We explored the signaling pathways downstream of Itgb3 using an additional in vivo shRNA screen and identified Syk as a critical mediator of Itgb3 activity in leukemia. Finally, we confirmed that Itgb3 is dispensable for normal hematopoiesis and required for leukemogenesis using the Itgb3 knockout mouse model. Our results establish the significance of the Itgb3 signaling pathway as a potential therapeutic target in AML, and demonstrate the utility of in vivo RNA interference screens. We examined the effect of Itgb3 knockdown by gene expression profiling in primary leukemia cells.

2013-04-24 | E-GEOD-46307 | biostudies-arrayexpress

Gene expression analysis of EpH4 cell monolayers following TGF-β3 treatment

Project description:EpH4 cell monolayers were treated with 1 ng/ml TGF-β3 or vehicle for 24 hours. The experiment was performed three independent times, with 3 wells per condition in each experiment. Keywords: Expression profiling by array

2015-10-01 | GSE62126 | GEO

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