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MiR-126 over-expression in highly metastatic LM2 breast cancer cells

ABSTRACT: miR-126 were over-expressed using the miR-Vec system in highly metastatic LM2 cells. The LM2 cell line are described in detail in Minn et al. Nature 2005 This approach was used to conduct an unbiased search for specific miR-126 target genes in breast cancer cells. 4 Samples

ORGANISM(S): Homo sapiens

SUBMITTER: Png KJ

PROVIDER: S-ECPF-GEOD-23905 | biostudies-other | 2012 Jan

REPOSITORIES: biostudies-other

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miR-126 over-expression in highly metastatic LM2 breast cancer cells.

Project description:miR-126 were over-expressed using the miR-Vec system in highly metastatic LM2 cells. The LM2 cell line are described in detail in Minn et al. Nature 2005 This approach was used to conduct an unbiased search for specific miR-126 target genes in breast cancer cells.

2011-12-16 | GSE23905 | GEO

miR-126 over-expression in highly metastatic LM2 breast cancer cells.

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Gene expression profilling of poorly metastatic MDA cells and highly metastatic LM2 cells

Project description:Comparison of gene expression between the breast cancer cell line MDA-MB-231 and its highly metastatic deriviate LM2 cells (described in Minn et al., Nature 2005). Results hilghlights potential metastasis promoting and suppressing genes. 4 Samples

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miR-126 and miR-126* repress recruitment of mesenchymal stem cells and inflammatory monocytes to inhibit breast cancer metastasis.

Project description:The tumour stroma is an active participant during cancer progression. Stromal cells promote tumour progression and metastasis through multiple mechanisms including enhancing tumour invasiveness and angiogenesis, and suppressing immune surveillance. We report here that miR-126/miR-126(*), a microRNA pair derived from a single precursor, independently suppress the sequential recruitment of mesenchymal stem cells and inflammatory monocytes into the tumour stroma to inhibit lung metastasis by breast tumour cells in a mouse xenograft model. miR-126/miR-126(*) directly inhibit stromal cell-derived factor-1 alpha (SDF-1?) expression, and indirectly suppress the expression of chemokine (C-C motif) ligand 2 (Ccl2) by cancer cells in an SDF-1?-dependent manner. miR-126/miR-126(*) expression is downregulated in cancer cells by promoter methylation of their host gene Egfl7. These findings determine how this microRNA pair alters the composition of the primary tumour microenvironment to favour breast cancer metastasis, and demonstrate a correlation between miR-126/126(*) downregulation and poor metastasis-free survival of breast cancer patients.

| S-EPMC3672398 | biostudies-literature

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Gene expression profilling of poorly metastatic MDA cells and highly metastatic LM2 cells.

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Parental MeWo and highly metastatic LM2 human melanoma cell line derivatives with or without miR-199a or miR-1908

Project description:Human melanoma MeWo cells and their respective LM2 metastatic derivatives, generated through in vivo selection, were transcriptomically profiled in the context of miR-199a and miR-1908 gain- and loss-of-function in order to identify putative target genes for these miRNAs, MeWo cells and their respective LM2 metastatic derivatives in the context of miR-199a and miR-1908 gain- and loss-of-function

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Evaluation of the Expression Level and Hormone Receptor Association of miR-126 in Breast Cancer.

Project description:Breast cancer is a major cause of cancer-related death in women worldwide. miRNAs are new players of breast tumorigenesis, used as diagnostic and prognostic biomarkers. Among various miRNAs, miR-126 has been proposed to have a tumor suppressive role in HER2 positive cancer. However, to have a better understanding of its role, further validation is required. The aim of this study was evaluating miR-126 expression level in breast cancer tissues and investigating its potential association with HER2, estrogen and progesterone receptors. miR-126 expression level was measured in 108 specimens including 78 malignant and 30 normal samples using RT-qPCR. The outcome was statistically analyzed. In silico studies were performed to find the potential mechanism of action, through which miR-126 imposes its function. Down-regulation of miR-126 was observed in tumor samples, as compared to the matched normal tissues. Down-regulation of miR-126 was also associated significantly with the absence of estrogen receptor in malignant samples. No association between miR-126 expression and HER2 status was observed. Our in silico analyses showed the possible role of Crk, PI3K and Ras proto-oncogenes in breast cancer tumorigenesis. miR-126 is significantly down-regulated in breast cancer tissues. Statistically, it showed no correlation with HER2 positivity. However, the association between lower miR-126 and estrogen receptor negativity was observed.

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Parental MeWo and highly metastatic LM2 human melanoma cell line derivatives with or without miR-199a or miR-1908

2013-02-10 | GSE35668 | GEO

Lung metastatic derivative LM2 cells with and without miR-335

Project description:the LM2 breast cancer cell line is an in vivo derived line from the MDA-MB-231 parental line. this LM2 line has been transduced either with a short hairpin control or miR-335 expression vector. Keywords: breast cancer, metastasis, miRNA

2008-01-01 | GSE9586 | GEO

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