Effect of matrix deprivation on breast cancer cells Part-1
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE108817 | GEO | 2019/06/30
REPOSITORIES: GEO
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Project description:Gene expression analysis of MDA-MB-231 breast cancer cells cultured in suspension {and stably expressing control shRNA, shPHLPP2 or GFP-Akt DD (GFP-HA-Akt-T308D S473D)}. Results provide insights into regulation of molecular pathways by PHLPP2 and Akt signaling in matrix deprived condition.
2019-06-30 | GSE108818 | GEO
Project description:Matrix-deprivation stress leads to cell-death by anoikis, whereas overcoming anoikis is critical for cancer metastasis. Work from our lab and others has identified a crucial role for the cellular energy sensor AMPK in anoikis-resistance, highlighting a key role for metabolic reprogramming in stress survival. Protein synthesis is a major energy-consuming process that is tightly regulated under stress. Although an increase in protein synthesis in AMPK-depleted experimentally-transformed MEFs has been associated with anoikis, the status and regulation of protein translation in epithelial-origin cancer cells facing matrix-detachment remains largely unknown. Our study shows that protein translation is mechanistically abrogated at both initiation and elongation stages by the activation of the unfolded protein response (UPR) pathway and inactivation of elongation factor eEF2, respectively. Additionally, we show inhibition of the mTORC1 pathway known for regulation of canonical protein synthesis. We further functionally assay this inhibition using SUnSET assay, which demonstrates repression of global protein synthesis in MDA-MB-231 and MCF7 breast cancer cells when subjected to matrix-deprivation. In order to gauge the translational status of matrix-deprived cancer cells, we undertook polysome profiling. Our data revealed reduced but continuous mRNA translation under matrix-deprivation stress. An integrated analysis of transcriptomic and proteomic data further identifies novel targets that may aid cellular adaptations to matrix-deprivation stress and can be explored for therapeutic intervention.
2023-06-14 | GSE234460 | GEO
Project description:1. Quantitative Proteomics: MDA-MB-231, MDA-MB-468, and MCF12A cells were treated with DMSO (vehicle control) or SU056 (novel small molecule drug candidate). Quantitative proteomics analysis was performed on cell lysates. 2. Cellular Thermal Shift Assay (CETSA): MDA-MB-231 cells were treated with DMSO or SU056 and incubated at different temperatures and protein differences in the resulting soluble and insoluble fractions were determined.3. Cellular Thermal Shift Assay (CETSA): MDA-MB-231 YBOX1 KD cells were treated with DMSO or SU056 and incubated at different temperatures and protein differences in the soluble fractions were determined.
2024-04-04 | PXD042380 | Pride
Project description:Intercellular communication is critical for integrating complex signals in multicellular eukaryotes. Vascular endothelial cells and T lymphocytes closely interact during the recirculation and trans-endothelial migration of T cells. In addition to direct cell-cell contact, we show that T cell derived extracellular vesicles can interact with endothelial cells and modulate their cellular functions. Thrombospondin-1 and its receptor CD47 are expressed on exosomes/ectosomes derived from T cells, and these extracellular vesicles are internalized and modulate signaling in both T cells and endothelial cells. Extracellular vesicles released from cells expressing or lacking CD47 differentially regulate activation of T cells induced by engaging the T cell receptor. Similarly, T cell-derived extracellular vesicles modulate endothelial cell responses to vascular endothelial growth factor and tube formation in a CD47-dependent manner. Uptake of T cell derived extracellular vesicles by recipient endothelial cells globally alters gene expression in a CD47-dependent manner. CD47 also regulates the mRNA content of extracellular vesicles in a manner consistent with some of the resulting alterations in target endothelial cell gene expression. Therefore, the thrombospondin-1 receptor CD47 directly or indirectly regulates intercellular communication mediated by the transfer of extracellular vesicles between vascular cells. Treatment with B6H12 antibody inhibited co-immunoprecipitation of EGFR with CD47 and inhibited EGF-induced EGFR tyrosine phosphorylation. B6H12 treatment of bCSC also suppressed asymmetric cell division and cell proliferation and up-regulated caspase 3/7 activity. Correspondingly, caspase-7 cleavage in human breast cancers correlated with CD47 expression. Our data shows that B6H12 specifically targets bCSCs but not differentiated cancer cells, and this CD47 signaling is independent of SIRPα. Three replicates of each condition were generated. Three replicates of each MDA-231 attached cells (differentiated), MDA-231 in suspension cells (bCSC), MDA-231 in suspension cells (bCSC) treated with Control Antibody and MDA-231 in suspension cells (bCSC) treated with B6H12 Antibody.
2016-04-01 | E-GEOD-67966 | biostudies-arrayexpress
Project description:Analysis of breast cancer MDA-MB-231 cells stably over-expressing SUV420H2, a histone H4K20 methyltransferase. Several genes were significantly up- or down-regulated. Results provide insight into the molecular mechanism by which H4K20me3 contributes to gene expression. SUV420H2 stably over-expressing MDA-MB-231 cells were cloned. Then total RNA was extracted from the SUV420H2 over-expressing cells and the parental MDA-MB-231 cells.
2015-04-15 | E-GEOD-55947 | biostudies-arrayexpress
Project description:Analysis of breast cancer MDA-MB-231 cells stably over-expressing SUV420H2, a histone H4K20 methyltransferase. Several genes were significantly up- or down-regulated. Results provide insight into the molecular mechanism by which H4K20me3 contributes to gene expression. SUV420H2 stably over-expressing MDA-MB-231 cells were cloned. Then total RNA was extracted from the SUV420H2 over-expressing cells and the parental MDA-MB-231 cells.
2015-04-15 | E-GEOD-56912 | biostudies-arrayexpress
Project description:CD44, an adhesion molecule that binds to extracellular matrix, primarily to hyaluronan (HA), has been implicated in cancer cell migration, invasion, and metastasis. CD44 has also recently been recognized as a marker for stem cells of several types of cancer. However, the roles of CD44 in the development of bone metastasis still remain unclear. To explore this issue, we established the MDA-MB-231 human breast cancer cells stably expressing short hairpin RNA against CD44. The CD44-knockdown MDA-MB-231 cells (MDA-MB-231 shCD44-2 and shCD44-3) were analyzed. As control, MDA-MB-231 cells stably expressing shRNA against firefly luciferase (shLuc) were used. Total of three samples. No replicates.
2013-04-24 | E-GEOD-45613 | biostudies-arrayexpress
Project description:To evaluate changes in gene expression in MDA-MB-231 cancer cells upon interaction with different extracellular matrices Gene expression in MDA-MB-231 cells was assayed after overnight incubation of the cells on gelatin or dense fibrillar collagen (HDFC) matrices at the presence or absence of serum in tissue culture medium. Five repeats were performed
2015-01-16 | E-GEOD-53104 | biostudies-arrayexpress
Project description:We used microarrays to investigate gene expression changes induced by the inhibition of RRAS2 expression using shRNA techniques to stably knockdown the endogenous transcripts of this GTPase in human MDA-MB-231-Luc cells. MDA-MB-231-Luc shControl (MDA-Control) and RRAS2-deficient (KDRRAS2.p1) in exponential growth phase were selected for RNA extraction and and hybridization on Affymetrix microarrays.
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Project description:Suspension of breast cancer cells MDA-MB-231 Transcriptome
| PRJNA412173 | ENA