Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA219097 | ENA |
REPOSITORIES: ENA
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Project description:MicroRNAs (miRNAs, micro ribonucleic acids) are pivotal post-transcriptional regulators of gene expression. These endogenous small non-coding RNAs play significant roles in tumorigenesis and tumor progression. miR-142-3p expression is dysregulated in several breast cancer subtypes. We aimed at investigating the role of miR-142-3p in breast cancer cell invasiveness. Supported by transcriptomic Affymetrix array analysis and confirmatory investigations at the mRNA and protein level, we demonstrate that overexpression of miR-142-3p in MDA-MB-231, MDA-MB-468 and MCF-7 breast cancer cells leads to downregulation of WASL (Wiskott-Aldrichsyndrome-like, protein: N-WASP), Integrin-aV, RAC1, and CFL2, molecules implicated in cytoskeletal regulation and cell motility. ROCK2, IL6ST, KLF4, PGRMC2 and ADCY9 were identified as additional targets in a subset of cell lines. Decreased matrigel invasiveness was associated with the miR-142-3p-induced expression changes. Confocal immunofluorescence microscopy, nanoscale atomic force microscopy and digital holographic microscopy revealed a change in cell morphology as well as a reduced cell volume and size. A more cortical actin distribution and a loss of membrane protrusions were observed in cells overexpressing miR-142-3p. Luciferase activation assays confirmed direct miR-142-3p-dependent regulation of the 3'-untranslated region of ITGAV and WASL. siRNA-mediated depletion of ITGAV andWASL resulted in a significant reduction of cellular invasiveness, highlighting the contribution of these factors to the miRNA-dependent invasion phenotype. While knockdown of WASL significantly reduced the number of membrane protrusions compared to controls, knockdown of ITGAV resulted in a decreased cell volume, indicating differential contributions of these factors to the miR-142-3p-induced phenotype. Our data identify WASL, ITGAV and several additional cytoskeleton associated molecules as novel invasion-promoting targets of miR-142-3p in breast cancer.
2015-11-16 | GSE50829 | GEO
Project description:MiRNAs have been shown to alter both protein expression and secretion in different cellular contexts. By combining in vitro, in vivo and in silico techniques, we demonstrated that overexpression of pre-miR-1307 reduced the ability of breast cancer cells to induce endothelial cell sprouting and angiogenesis. However, the molecular mechanism behind this and the effect of the individual mature miRNAs derived from pre-miR-1307 on protein secretion and is largely unknown. Here, we overexpressed miR-1307-3p|0, -3p|1 and 5p|0 in MDA-MB-231 breast cancer cells and assessed the impact of miRNA overexpression on protein secretion by Mass Spectrometry. Unsupervised hierarchical clustering revealed a distinct phenotype induced by overexpression of miR-1307-5p|0 compared to the controls and to the 5’isomiRs derived from the 3p-arm. Together, our results suggest different impacts of miR-1307-3p and miR-1307-5p on protein secretion which is in line with our in vitro observation that miR-1307-5p, but not the isomiRs derived from the 3p-arm reduce endothelial cell sprouting in vitro. Hence these data support the hypothesis that miR-1307-5p is at least partly responsible for impaired vasculature in tumors overexpressing pre-miR-1307.
2024-12-11 | PXD041087 | Pride
Project description:To investigate the effects of breast cancer derived EVs on liver metabolism,we inoculated MDA-MB-231,231 /Rab27A KD and 231 /miR-9 KO cells into subcutaneous tumor in NSG mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of liver from mice xenografted MDA-MB-231 cells (tumor bearing) or MDA-MB-231/Rab27A KD cells (231/Rab27A KD) or MDA-MB-231 /miR-9 KO (231/miR-9 KO) and tumor free mice.
2024-08-31 | GSE222707 | GEO
Project description:Using microarray, we compared miRNAs expression profiles of MDA-MB-231 cells transfected with myocardin and empty vector (pcDNA3.1) and found that 25 miRNAs were significantly changed in myocardin-transfected groups (17 up-regulated and 9 down-regulated miRNAs). Moreover, we showed that 18 of 25 miRNAs significantly regulated by myocardin were inhibited by ERα in MDA-MB-231 cells. In addition,through a microarray approach, we identify the subset of miRNAs modulated by ERα in MDA-MB-231 cells. Our results determined that ERα may function as tumor-promoter through down-regulating expression of 3 miRNAs (miR-26b, miR-146a and miR-331-3p) in MDA-MB-231 cells.
2014-10-01 | GSE44139 | GEO
Project description:We have employed whole genome microarray to identify changes in gene expression in MDA-MB-231 cells transfected with hsa-miR-205-5p and hsa-miR-214-3p compared to scrambled miRNA precursors at 72 hours after transfection.
2020-05-31 | GSE148847 | GEO
Project description:The project profiled the expression patterns in hypoxia induced secretomes between MDA-MB-231 parental and MDA-MB-231 Bone Tropic (BT) breast cancer cell lines which have been previously generated by Massague and colleagues (Kang et al. Cancer Cell 2003).
2017-03-29 | MSV000080797 | MassIVE
Project description:Aurora Kinase B and ZAK interaction model
Equivalent of the stochastic model used in "Network pharmacology model predicts combined Aurora B and ZAK inhibition in MDA-MB-231 breast cancer cells" by Tang et. al. 2018.
The only difference is cell division and partitioning of the components, which are available in the original model for SGNS2.
2024-09-02 | BIOMD0000000940 | BioModels
Project description:Bone morphogenetic protein 4 (BMP4) is a remarkably powerful inhibitor of breast cancer cell proliferation, but is also able to induce breast cancer cell migration in certain cellular contexts. Previous data demonstrate that BMP4 controls the transcription of a variety of protein coding genes, but not much is known about microRNAs (miRNA) regulated by BMP4. In this study, miRNA expression patterns following BMP4 treatment were determined in one mammary epithelial and seven breast cancer cell lines using microarrays. The analysis identified 20 to 128 differentially expressed miRNAs in individual cell lines with emphasis on upregulation over downregulation. Four miRNAs (miR-16-5p, miR-106b-5p, miR-23a-3p and miR-23b-3p) were commonly induced in a subset of breast cancer cells upon BMP4 treatment and inhibition of their expression resulted in an increase in BT-474 cell number, indicating that they possess tumor suppressive properties. Yet no major change was detected when the cells were simultaneously treated with BMP4, and thus these miRNAs do not act as the main mediators of BMP4-induced growth reduction. MiR-16-5p and miR-106b-5p were elevated in MDA-MB-231 cells that respond to BMP4 with increased migration. Their inhibition, in combination with BMP4 treatment, resulted in enhanced MDA-MB-231 cell migration, suggesting that miR-16-5p and miR-106b-5p are engaged in BMP4-induced motility. Taken together, we have shown for the first time that in breast cancer cells BMP4 induces variable miRNA expression patterns.
2015-12-01 | GSE70480 | GEO
Project description:To identify gene expression changes associated with treatment of EV that carry high levels of miR-105 (from MDA-MB-231 and MCF10A/miR-105 cells) in human breast tumor derived CAF, we analyzed RNA isolated from PBS- or EV-treated CAF. Gene expression in CAF treated with EV from MDA-MB-231 or MCF10A/miR-105 cells was compared to cells treated with PBS or EV from MCF10A cells, both of which served as controls in this experiment.
2018-02-11 | GSE106503 | GEO
Project description:Using microarray, we compared miRNAs expression profiles of MDA-MB-231 cells transfected with myocardin and empty vector (pcDNA3.1) and found that 25 miRNAs were significantly changed in myocardin-transfected groups (17 up-regulated and 9 down-regulated miRNAs). Moreover, we showed that 18 of 25 miRNAs significantly regulated by myocardin were inhibited by ERM-NM-1 in MDA-MB-231 cells. In addition,through a microarray approach, we identify the subset of miRNAs modulated by ERM-NM-1 in MDA-MB-231 cells. Our results determined that ERM-NM-1 may function as tumor-promoter through down-regulating expression of 3 miRNAs (miR-26b, miR-146a and miR-331-3p) in MDA-MB-231 cells. There are 4 samples in this experiment (pcDNA3.1-transfected, myocardin-transfected, ERM-NM-1-transfected, myocardin plus ERM-NM-1 co-transfecteded groups) and each sample was replicated 3 times. The vector-pcDNA3.1 was used as control.
2014-10-01 | E-GEOD-44139 | biostudies-arrayexpress