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Gene expression in WT and podoplanin (PDPN)-deficient MEFs

ABSTRACT: MEFs were grown from WT and PDPN-deficient mouse embryos and gene expression was analyzed. The aim was to determine whether a lack of PDPN caused significant global changes in gene expression in primary fibroblasts. Here, we performed a microarray on WT and PDPN-deficient mouse embryonic fibroblasts to determine whether there were signficiant underlying changes in gene expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE62081 | GEO | 2014/10/07

SECONDARY ACCESSION(S): PRJNA263168

REPOSITORIES: GEO

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Gene expression in WT and podoplanin (PDPN)-deficient MEFs

Project description:MEFs were grown from WT and PDPN-deficient mouse embryos and gene expression was analyzed. The aim was to determine whether a lack of PDPN caused significant global changes in gene expression in primary fibroblasts. Here, we performed a microarray on WT and PDPN-deficient mouse embryonic fibroblasts to determine whether there were signficiant underlying changes in gene expression. Two replicates each of WT and PDPN KO MEFs from C57BL6/J mice

2014-10-07 | E-GEOD-62081 | biostudies-arrayexpress

Gene expression data of nasopharyngeal carcinoma (NPC) cell and Podoplanin (PDPN) siRNA treatment

Project description:Podoplanin, a transmembrane sialomucin-like glycoprotein, is now widely used as a marker for lymphatic endothelial cells and fibroblastic reticular cells in lymphoid organs, but its study in nasopharyngeal carcinoma (NPC) is still limited. The aims of this study were t characterize the role of PDPN in NPC. Our results showed that PDPN was expressed in most TW01 NPC cells. PDPN knockdown by siRNA decreased NPC cell proliferation, migration, and invasion. Knocking down PDPN results in suppression of NPC cell proliferation, migration, and invasion. PDPN may serve as a potential chemotherapeutic target for NPC treatment in the future.

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Mus musculus

Project description:Gene expression in WT and podoplanin (PDPN)-deficient MEFs

| PRJNA263168 | ENA

Comparison of tenascin-C proficient versus tenascin-C deficient Mouse Embryonic Fibroblasts (MEFs)

Project description:In order to investigate what signalling pathways are turned on by tenascin-C, we generated Mouse Embryonic Fibroblasts (MEFs) deficient for tenascin-C and compared their gene expression profile to MEFs proficient for tenascin-C. TNC-KO MEFs as well as WT MEFs in which tenascin-C was knocked-down (following stable transfection of a short hairpin RNA) were compared to WT MEFs (expressing strong endogenous levels of tenascin-C).

2011-02-22 | E-GEOD-23547 | biostudies-arrayexpress

Podoplanin-expressing macrophages (PoEMs) promote lymphangiogenesis and favour lymphatic metastasis in breast cancer

Project description:RNAseq was performed on PoEMs (CD11b+, F4/80+, PDPN+) vs. non-PoEMs (CD11b+, F4/80+, PDPN-) sorted from orthotopically inoculated 4T1 tumors in WT mice.

2019-10-03 | GSE126722 | GEO

Microarray analysis of gene expression in ATM-deficient MEFs

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WT and Mk2/3 KO MEFs response to etoposide

Project description:Primary mouse embryonic fibroblasts (MEFs) from wt and MK2/3 KO mice were treated with 20µM etoposide.

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Quantification of PIPs species in mouse embryonic fibroblasts (MEFs) during autophagosome formation.

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Inflammation-Driven Carcinogenesis is Mediated through STING [MEFs]

Project description:Chronic stimulation of innate immune pathways by microbial agents or damaged tissue is known to promote inflammation-driven tumorigenesis by unclarified mechanisms1-3. Here we demonstrate that mutagenic 7,12-dimethylbenz(a)anthracene (DMBA), etoposide or cisplatin induces nuclear DNA leakage into the cytosol to intrinsically activate STING (Stimulator of Interferon Genes) dependent cytokine production. Inflammatory cytokine levels were subsequently augmented in a STING-dependent extrinsic manner by infiltrating phagocytes purging dying cells. Consequently, STING-/- mice, or wild type mice adoptively transferred with STING-/- bone marrow, were almost completely resistant to DMBA-induced skin carcinogenesis compared to their wild type counterparts. Our data emphasizes, for the first time, a role for STING in the induction of cancer, sheds significant insight into the causes of inflammation-driven carcinogenesis, and may provide therapeutic strategies to help prevent malignant disease Total RNA obtained from wild type murine embryonic fibroblasts (WT MEFs), STING deficient MEFs (SKO), Trex1 deficient MEFs (TKO), and both STING and Trex1 deficient MEFs (STKO) treated with DMBA and examined cytokine production by these cells.

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