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The melanoma cell line MDA-MB-435 adhesome in long-term culture and its comparison to the adhesome upon integrin αV knockdown

ABSTRACT: Using mass spectrometry–based proteomics, we analysed the components of integrin adhesion complexes of MDA-MB-435S cells and two MDA-MB-435S-derived integrin αV-specific shRNA-expressing cell clones. Among integrins, we detected αV and β5 integrin subunits in the MDA-MB-435S adhesome, thus showing that in long term culture these cells use preferentially integrin αVβ5 for adhesion. Our data represents the first published adhesome of αVβ5 integrin heterodimer.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Melanocyte, Cell Culture

DISEASE(S): Melanoma

SUBMITTER: Mladen Paradzik

LAB HEAD: Andreja Ambriović-Ristov

PROVIDER: PXD016837 | Pride | 2020-02-17

REPOSITORIES: Pride

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			Action	DRS
	20170307_JH_04.DAT	Other
	20170307_JH_04.raw	Raw
	20170307_JH_05.DAT	Other
	20170307_JH_05.raw	Raw
	20170307_JH_06.DAT	Other

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1 - 5 of 17

Publications

KANK2 Links αVβ5 Focal Adhesions to Microtubules and Regulates Sensitivity to Microtubule Poisons and Cell Migration.

Paradžik Mladen M Humphries Jonathan D JD Stojanović Nikolina N Nestić Davor D Majhen Dragomira D Dekanić Ana A Samaržija Ivana I Sedda Delphine D Weber Igor I Humphries Martin J MJ Ambriović-Ristov Andreja A

Frontiers in cell and developmental biology 20200303

Integrins are heterodimeric glycoproteins that bind cells to extracellular matrix. Upon integrin clustering, multimolecular integrin adhesion complexes (IACs) are formed, creating links to the cell cytoskeleton. We have previously observed decreased cell migration and increased sensitivity to microtubule (MT) poisons, paclitaxel and vincristine, in the melanoma cell line MDA-MB-435S upon transfection with integrin αV-specific siRNA, suggesting a link between adhesion and drug sensitivity. To elu ...[more]

PMID: 32195252

Similar Datasets

Gene expression analysis in CITED2 knockdown MDA-MB-231 human breast cancer cells.

Project description:The goal of this experiment is to explore the mechanism behind CITED2 (a non-DNA binding transcriptional co-activator) metastatic action by comparing gene expression changes between shScramble and shCITED2-expressing MDA-MB-231 cells.

2017-01-14 | E-MTAB-4267 | biostudies-arrayexpress

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

human breast cancer cell line LC-MS/MS

Project description:Triple-negative breast cancer (TNBC) is the most aggressive type with poor prognosis among the breast cancers and has a high population of cancer stem cells (CSCs) which are main target to cure and inhibit TNBC. In this study, we analyzed the CSC-related proteome alteration by NEDD4 knockdown in CSC-abundant MDA-MB-231 cells by LC-MS/MS analysis.

2021-09-09 | PXD020585 | Pride

Characterization of macrophage - cancer cell crosstalk in estrogen receptor positive and triple-negative breast cancer

Project description:We performed whole transcriptome sequencing of human monocytes that were co-cultured with estrogen receptor positive (ER+) or triple-negative (TNBC) breast cancer cell lines and studied the biological responses related to the differential gene activation in both cell types to understand how different cancer cells educate host cells to support tumor growth To characterize the differences in macrophage activation under the influence of either ER+ or TNBC breast cancer cells, we cultured freshly isolated human peripheral monocytes with two breast cancer cell lines (T47D, ER+ and MDA-MB-231, TNBC) in an in vitro transwell co-culture assay. The transwell setting allowed us to investigate the effect of soluble mediators on macrophage activation since direct cell contact of these cells was inhibited by a (PET) membrane (pore size 0.4âÎ¼m).

2015-11-19 | E-GEOD-75130 | biostudies-arrayexpress

Differential transcript stability measurements in MDA-MB-231 vs. MDA-LM2 cells

Project description:We performed whole-genome stability measurements for MDA-MB-231 and its highly metastatic derivative MDA-LM2. Our goal was to identify post-transcriptonal regulons that are deregulated en route to higher metastatic capacity. Cells were pulsed with 4-thiouridine for 2 hours and then RNA was extracted at 0, 2, 4, and 7 hr time-points in quadruplicate from each cell line. 4sU labeling followed by RNA-seq was then used to measure the abundance of transcripts in each population. A decay rate was estimated based on the rate at which transcript abundance was reduced at these time-points.

2014-07-24 | E-GEOD-49608 | biostudies-arrayexpress

Detection and isolation of circulating tumor cells from breast cancer patients using CUB domain-containing protein 1 (CDCP1) Detection and isolation of circulating tumor cells from breast cancer patients using CUB domain-containing protein 1 (CDCP1) Detection and isolation of circulating tumor cells from breast cancer patients using CUB domain-containing protein 1 (CDCP1)

Project description:Circulating tumor cells (CTCs) and disseminated tumour cells with mesenchymal traits are difficult to detect by epithelial marker proteins. Particularly, triple negative breast cancers (TNBC) that are prone to therapy failure release a subpopulation of circulating tumour cells (CTCs) with mesenchymal traits. To provide tools that support their detection and analysis, the cell line BC-M1 established from disseminated tumour cells in the bone marrow of a breast cancer patient and a bone metastasis subline of MDA-MB-231 were analysed. Mass spectrometry analysis revealed high levels of CUB domain-containing protein 1 (CDCP1) in BC-M1. CDCP1 was found in other carcinoma cell lines (MDA-MB-231, MDA-MB-468) and other DTC cell lines (LC-M1, PC-E1) as well. Peripheral blood mononuclear cells were virtually negative for CDCP1 by Western Blot and immunofluorescent staining. Presence of CDCP1 in CTCs was confirmed by CellSearch. Here, CDCP1 positive CTCs were detected in eight of 30 analysed breast cancer patients. For the isolation of CTCs from the blood of breast cancer patients, we established a sandwich magnetic-activated cell sorting (MACS). The extracellular domain of CDCP1 served for cell catching and the cytoplasmic domain of CDCP1 for immunofluorescent detection of CDCP1 in CTCs. We showed that the MACS approach is suitable for the isolation of EpCam/keratin negative breast cancer cells from the blood and isolated CDCP1 positive CTCs from breast cancer patients by MACS. Hence, our approach is particularly suited for the detection and isolation of CTCs from TNBC when low EpCam or keratin levels limit the application of conventional approaches.

2023-03-20 | PXD035203 | Pride

The tongue squamous carcinoma cell line Cal27 primarily employs integrin α6β4-containing type II hemidesmosomes for adhesion which contribute to anticancer drug sensitivity

Project description:Integrins are heterodimeric cell surface glycoproteins used by cells to bind to the extracellular matrix (ECM) and regulate tumor cell proliferation, migration and survival. A causative relationship between integrin expression and resistance to anticancer drugs has been demonstrated in different tumors, including head and neck squamous cell carcinoma. Using a Cal27 tongue squamous cell carcinoma model, we have previously demonstrated that de novo expression of integrin αVβ3 confers resistance to several anticancer drugs (cisplatin, mitomycin C and doxorubicin) through a mechanism involving downregulation of active Src, increased cell migration and invasion. In the integrin αVβ3 expressing Cal27-derived cell clone 2B1, αVβ5 expression was also increased, but unrelated to drug resistance. To identify the integrin adhesion complex (IAC) components that contribute to the changes in Cal27 and 2B1 cell adhesion and anticancer drug resistance, we isolated IACs from both cell lines. Mass spectrometry (MS)-based proteomics analysis indicated that both cell lines preferentially use integrin α6β4, which is classically found in hemidesmosomes. The anticancer drug resistant cell clone 2B1 demonstrated an increased level of α6β4 accompanied with increased deposition of a laminin-332-containing ECM. Immunofluorescence and electron microscopy demonstrated the formation of type II hemidesmosomes by both cell types. Furthermore, suppression of α6β4 expression in both lines conferred resistance to anticancer drugs. Taken together, our results identify a key role for α6β4-containing type II hemidesmosomes in regulating anticancer drug sensitivity.

2022-02-16 | PXD028810 | Pride

Targeting the SIN3A-PF1 Interaction inhibits Epithelial to Mesenchymal Transition and Maintenance of a Stem Cell Phenotype in Triple Negative Breast Cancer (MNase-seq)

Project description:Triple negative breast cancer (TNBC) is characterized by a poorly differentiated phenotype and limited treatment options. Aberrant epigenetics in this subtype represent a potential therapeutic opportunity, but a better understanding of the mechanisms contributing to the TNBC pathogenesis is required. The SIN3 molecular scaffold performs a critical role in multiple cellular processes, including epigenetic regulation, and has been identified as a potential therapeutic target. Using a competitive peptide corresponding to the SIN3 interaction domain of MAD (Tat-SID), we investigated the functional consequences of selectively blocking the paired amphipathic helix (PAH2) domain of SIN3. Here, we report the identification of the SID-containing adaptor PF1 as a factor required for maintenance of the TNBC stem cell phenotype and epithelial to mesenchymal transition (EMT). Tat-SID peptide blocked the interaction between SIN3A and PF1, leading to epigenetic modulation and transcriptional downregulation of TNBC stem cell and EMT markers. Importantly, Tat-SID treatment led to a reduction in primary tumor growth and disseminated metastatic disease in vivo. In support of these findings, knockdown of PF1 expression phenocopied treatment with Tat-SID both in vitro and in vivo. These results demonstrate a critical role for a complex containing SIN3A and PF1 in TNBC and provide a rational for its therapeutic targeting. Mononucleosomes from MDA-MB-231 cells were isolated and ChIP with H3K4me3 antibody. DNA from Input and ChIP samples was purified and sequenced on Illumina Hiseq.

2015-11-02 | E-GEOD-73869 | biostudies-arrayexpress

A panel of breast cell lines

Project description:RNA expression patterns of breast cell lines were compared with a breast cell line mixed reference. Gene expression profiles of 52 individual breast cell lines relative to a breast cell line reference mix containing equal amounts of 10 breast cell lines.

2013-02-22 | E-GEOD-44552 | biostudies-arrayexpress

The effect of cannabinoid receptor agonists on triple-negative breast cancer cell line (MDA-MB-231)

Project description:The endocannabinoid system (ECS) provides regulatory functions in several cellular and physiological processes. It has also been found to play a role in control of cancer development. Our group found that breast cancer cells responded to cannabinoid receptor (CB) agonist treatments. This leads the activation of CB receptors in breast cancer, which inhibited their growth. In addition, breast cancer cells also behaved differentially when they were exposed to combinations of both CB1 and CB2 agonists. The underlying mechanism of individual- or co- activation after CB agonist exposure is still unknown. Hence, we studied the impact of CB activation on cancer molecular signature by performing proteomic analysis after triple-negative breast cancer (MDA-MB-231) cells exposed to CB receptor agonists. In this study, ACEA and GW405833 were used as CB1 and CB2 receptor agonists, respectively.

2024-07-27 | PXD040666 | Pride

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