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Comparing breast tumor cell-induced gene expression in primary mammary fibroblasts from MEKK1-deficient mice to fibroblasts from MEKK1+/+ mice

ABSTRACT: This study examined the importance of intracellular kinase MEKK1 in breast tumor-induced on gene expression in non-tumor mammary cells. The hypothesis tested in this study was that the kinase MEKK1 regulates breast tumor cells-induced expression of fibroblast genes that change the tumor microenvironment to promote breast tumor progression to metastasis. Results reveal that MEKK1 regulates expression of chemokines and other genes in normal breast stroma cells that contribute to the development of a tumor microenvironment that promotes metastasis.

ORGANISM(S): Mus musculus

PROVIDER: GSE167130 | GEO | 2021/02/20

REPOSITORIES: GEO

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Comparing breast tumor cell-induced gene expression in primary mammary fibroblasts from MEKK1-deficient mice to fibroblasts from MEKK1+/+ mice

Project description:Comparing breast tumor cell-induced gene expression in primary mammary fibroblasts from MEKK1-deficient mice to fibroblasts from MEKK1+/+ mice

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Sphingosine kinase 2 in stromal fibroblasts creates a hospitable tumor microenvironment in breast cancer

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2020-01-01 | GSE136655 | GEO

Single-cell RNA-sequencing of murine breast tumor infiltrating immune cells isolated from the site of metastasis in wild-type and short-form Ron knockout mice

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Sphingosine kinase 2 in stromal fibroblasts creates a hospitable tumor microenvironment in breast cancer

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A role for the mitogen-activated protein kinase kinase kinase 1 in epithelial wound healing

Project description:The mitogen-activated protein kinase kinase (MEK) kinase 1 (MEKK1), also known as MAP3K1, mediates activin B (ActB) signals required for eyelid epithelium morphogenesis during mouse fetal development. The present study investigates the role of MEKK1 in epithelial wound healing, another activin-regulated biological process. In a skin wound model, injury markedly stimulates MEKK1 expression and activity, which are in turn required for the expression of genes involved in extracellular matrix (ECM) homeostasis. MEKK1 ablation or down-regulation by interfering RNA significantly delays skin wound closure and impairs activation of Jun NH2-terminal kinases, induction of plasminogen activator inhibitor (PAI)-1, and restoration of cell-cell junctions of the wounded epidermis. Conversely, expression of wild-type MEKK1 accelerates reepithelialization of full-thickness skin and corneal debridement wounds by mechanisms involving epithelial cell migration, a cell function that is partially abolished by neutralizing antibodies for PAI-1 and metalloproteinase III. Our data suggest that MEKK1 transmits wound signals, leading to the transcriptional activation of genes involved in ECM homeostasis, epithelial cell migration, and wound reepithelialization.

2022-07-13 | GSE201823 | GEO

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2014-07-04 | E-GEOD-47930 | biostudies-arrayexpress

Primary breast tumor-derived cellular models: characterization of tumorigenic, metastatic, and cancer-associated fibroblasts in dissociated tumor (DT) cultures

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