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Expression data from mir-100 overexpression two TNBC cell lines

ABSTRACT: Expression data from mir-100 overexpression two TNBC cell lines

PROVIDER: PRJNA493246 | ENA |

REPOSITORIES: ENA

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Expression data from mir-100 overexpression two TNBC cell lines

Project description:Utilizing a tetracyclineinducible lentivirus to elevate expression of miR100 in human cells, we found that increasing miR100 levels decreased the production of breast CSCs. This effect was correlated with an inhibition of cancer cell proliferation in vitro and in mouse tumor xenografts.Furthermore, miR100 induction in breast CSCs immediately upon their orthotopic implantation or intracardiac injection completely blocked tumor growth and metastasis formation. Then we wanted to indentify the target genes of mir100 in breast cancer cells. We used microarrays to detail the changes of gene expression after mir100 overexpression in two TNBC cell lines and identified distinct classes of down-regulated genes during this process.

2018-09-27 | GSE120513 | GEO

Expression data from ETV6-RUNX1-positive Reh leukemic cells after overexpression of miR-125b, miR-100 and miR-99a levels in different combinations

2013-06-27 | GSE46362 | GEO

Expression data from ETV6-RUNX1-positive Reh leukemic cells after overexpression of miR-125b, miR-100 and miR-99a levels in different combinations

Project description:Combined overexpression of miR-125b with miR-99a and/or miR-100 induced VCR resistance in ETV6-RUNX1-positive leukemic cells Reh. We used microarrays to detail the global changes in gene expression of Reh cells upon enforced expression of miR-125 per se compared with combination of overexpression of miR-125b, miR-100 and/or miR-99a MiR-99a and/or miR-100 were transiently overexpressed in stable miR-125b-expressing and stable scrambled miR-control-expressing Reh cells. Cellular resistance to VCR was determined by MTT assay after incubating the cells with 9 ng/mL VCR for 3 days. Changes in the gene expression pattern of Reh cells induced by miRNAs overexpression were measured using Affymetrix Arrays.

2013-06-27 | E-GEOD-46362 | biostudies-arrayexpress

TNF-α promotes TNBC aggressiveness by upregulating miR-5001-5p and inhibiting MNK2a–p38 MAPK signaling

Project description:Triple-negative breast cancer (TNBC) has a greater invasive and metastatic potential than non-TNBC, leading to a poorer prognosis because of the absence of viable therapeutic targets. Tumor necrosis factor-alpha (TNF-α), which is aberrantly activated in TNBC, plays a pivotal role in TNBC metastasis and progression. The ability of TNF-α to promote TNBC progression is unique when compared with its ability to promote non-TNBC progression; however, the underlying mechanism remains unclear. TNF-α specifically enhanced the invasive and metastatic potential of TNBC compared with that of non-TNBC. Analysis of the differentially expressed miRNAs showed that TNF-α upregulated miR-5001-5p expression in TNBC cells. The results of transcriptomic sequencing combined with subsequent verification analysis indicated that MNK2a was significantly downregulated following miR-5001-5p overexpression. Evidence from dual-luciferase reporter assays confirmed that miR-5001-5p bound to the MNK2a 3' UTR region and inhibited the activation of the p38 MAPK pathway. Our results provide novel insights into the molecular mechanism by which TNF-α promotes epithelial–mesenchymal transition in TNBC through the TNF-α–miR-5001-5p–MNK2a–p38 MAPK signaling axis, eventually enhancing the invasive and metastatic potential of TNBC. We discovered a novel mechanism of invasion and metastasis in TNBC whereby TNF-α upregulated the expression of miR-5001-5p, which downregulated MNK2a by binding to its 3' UTR region. This inhibited the activation of the p38 MAPK pathway, following which MNK2a promoted epithelial–mesenchymal transition in TNBC. This mechanism offers a theoretical basis for TNBC-targeted therapy and also serves as a novel therapeutic target.

2025-03-31 | GSE285618 | GEO

miR-200c induction in BT549 TNBC cells

Project description:miR-200c induction in BT549 TNBC cells

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Identification of miR-100 and miR-125b targets by AGO2 RIP-seq and RNA-seq after ectopic expression of miR-100 or miR-125b and evaluation of the TGFb expression signature in PANC-1 cells by RNA-seq

Project description:To identify targets post-transcriptionally regulated by miR-100 and miR-125b, we have performed AGO2 RIP-seq and RNA-seq following overexpression of the two miRNAs in PANC-1 cells. In addition, we have carried out RNA-seq following TGFb stimulus to evaluate changes in gene expression driven by TGFb.

2018-04-18 | GSE88757 | GEO

miR-975 overexpression effect on Drosophila cell lines

Project description:miR-975 overexpression effect on Drosophila cell lines

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miR-1,miR-122,miR-124 overexpression in 293T cells

Project description:miR-1,miR-122,miR-124 overexpression in 293T cells

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Expression data from global miR-100 overexpressing mice

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MicroRNA expression data from an epithelial-mesenchymal transition (EMT) model of triple negative breast cancer (TNBC).

Project description:Triple-negative breast cancer (TNBC) is the most aggressive form of breast cancer due to lack of effective targeted therapies. Here, we report that the expression of miR-4417 is suppressed during the progression of TNBC cells from non-malignant to the malignant stage. miR-4417 is localized to chromosome 1p36, a region with high loss of heterozygosity in multiple cancers, and its biogenesis is DICER-dependent. Low expression of miR-4417 is significantly associated with worse prognosis in TNBC patients, while overexpression of miR-4417 is sufficient to inhibit migration and tumorigenecity of TNBC cells in vitro. Overall, our findings suggest that miR-4417 exerts a tumor suppressive effect and thereby could serve as a prognostic biomarker and therapeutic tool against TNBC. We used microarrays to profile the global miRNA changes during EMT to identify putative tumor suppressors and prognostic biomarkers for TNBC.

2019-10-15 | GSE121657 | GEO

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