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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Activation of ER-alpha network in MMTV-Wnt/ILK mammary tumors

ABSTRACT: A transgenic mouse model, MMTV-Wnt/ILK, with mammary specific expression of both Wnt-1 and ILK, was generated by crossing the two mouse lines MMTV-Wnt-1 and MMTV-ILK. Affymetrix Mouse Exon chips were hybridized with material from four independent mammary tumors from each MMTV-Wnt-1 and MMTV-Wnt/ILK transgenic model, in order to identify possible signaling differences involved during increased tumor incidence. One-way ANOVA: MMTV-Wnt vs. MMTV-Wnt/ILK

ORGANISM(S): Mus musculus

SUBMITTER: Samuel Aparicio

PROVIDER: E-GEOD-19300 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Activation of ER-alpha network in MMTV-Wnt/ILK mammary tumors

Project description:A transgenic mouse model, MMTV-Wnt/ILK, with mammary specific expression of both Wnt-1 and ILK, was generated by crossing the two mouse lines MMTV-Wnt-1 and MMTV-ILK. Affymetrix Mouse Exon chips were hybridized with material from four independent mammary tumors from each MMTV-Wnt-1 and MMTV-Wnt/ILK transgenic model, in order to identify possible signaling differences involved during increased tumor incidence.

2010-06-16 | GSE19300 | GEO

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Project description:Activation of ER-alpha network in MMTV-Wnt/ILK mammary tumors

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Expression data from Integrin-linked kinase (ILK)-deficient epidermis

Project description:ILK is essential for proper development of hair follicles, and for epidermal integrity and repair after injury. To better understand the pathways modulated by ILK in the epidermis, we compared the transcriptomes of ILK-deficient and -expressing epidermis using microarray analyses. Ilktm1Star (with floxed Ilk alleles) and Tg(KRT14-cre)1Amc/J mice were bred, and the resulting mice were bred again with Ilktm1Star mice, to generate animals heterozygos for the KRT14-cre transgene and either heterozygous (ILK-expressing) or homozygous (ILK-deficient) for the floxed Ilk alleles. The epidermis of 3 day-old animals was harvested and used to prepare RNA for the microarrays. The animals used were littermates. RNA from the epidermis of five ILK-deficient and five ILK-expressing mice were used.

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Project description:Gene expression profiling of samples from normal virgin mammary glands, hyperplastic mammary glands, mamary tumors, and lung metastases from MMTV-Wnt-1 transgenic (TG) mice, and mammary tumors and lung metastases from MMTV-Neu trangenic (TG) mice Keywords: Array analysis, multi-step tumorigenesis, metastasis, MMTV-Wnt-1 trangenic mice, MMTV-Neu transgenic mice

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Role of ILK in cardiac regeneration

Project description:Two different mouse models of cardiac-specific ILK expression (ILKS343D and ILKR211A) were used to investigate the role of ILK in cardiac regeneration

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Project description:Two different mouse models of cardiac-specific ILK expression (ILKS343D and ILKR211A) were used to investigate the role of ILK in cardiac regeneration 4 groups with 3 mice (biological replicates) in each group with the total of 12 heart samples were used in this microarray experiment

2012-12-25 | E-GEOD-25729 | biostudies-arrayexpress

RNA sequencing of ILK-deficient hair follicle bulge stem cells

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An ILK/STAT3 pathway controls plasticity in a neural stem cell model of glioblastoma.

Project description:Glioblastomas (GBM) are driven by malignant neural stem-like cells that display extensive heterogeneity and phenotypic plasticity, which drives tumour progression and therapeutic resistance. Here we show that the nodal extracellular matrix-cell adhesion protein integrin-linked kinase (ILK) is a key determinant of phenotypic plasticity and the mesenchymal-like, invasive cell state in mouse GBM stem cells. We found that an ILK-STAT3 signalling pathway is required for plasticity that enables the transition of GBM stem cells to an astrocyte-like state both in vitro andin vivo. GBM cells genetically depleted of ILK become predominantly stabilised in a transcriptionally-defined progenitor-like state that is characterised by lack of response to differentiation cues and constitutive proliferation. Loss of ILK or interference with STAT3 impairs differentiation potential, reducing phenotypic plasticity of tumour cell populations; additionally, ILK loss causes a mesenchymal- to epithelial-like morphological transition and suppression of malignancy-associated features. Our work defines ILK as a central regulator of multiple GBM phenotypes including phenotypic plasticity and mesenchymal state.

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The gain-of-function AKT1E17K allele is oncogenic in mouse mammary gland

Project description:The gain-of-function mutation in the pleckstrin homology domain of AKT1 (AKT1E17K) occurs in lung and breast cancer. By use of human cellular models and of a AKT1E17K transgenic Cre-inducible murine strain (R26-AKT1E17K mice) we have demonstrated that AKT1E17K is a bona-fide oncogene for lung epithelial cells. However, the role of AKT1E17K in breast cancer remains to be determined. Here, we report the generation and the characterization of a MMTV-CRE;R26-AKT1E17K mouse strain that expresses the mutant AKT1E17K allele in the mammary epithelium. We observed that R26AKT1E17K;MMTV-Cre mice presented a variety of proliferative alterations of the mammary epithelium that were classified as adenosis with low-to-high grade dysplasia. In addition, AKT1E17K stimulates the development of mammary tumors with incidence of 43%. Tumors were morphologically classified as ductal adenocarcinoma of medium-high grade though subsequent immunoistochemical characterization suggested they were of basal-like origin, being PR-/HER2-/ERα+ and CK8-/CK10-/CK5+/CK14+. We also observed that tumors expressing mutant AKT1E17K presented activation of the downstream signaling axis GSK3/cyclin D1 in mammary epithelium, in parallel with increased proliferation rate as demonstrated by cell number count and measurement of Ki67. In conclusion, AKT1E17K is a bona fidae oncogene that is able to initiate tumors at high efficiency in murine mammary epithelium in vivo.

2022-06-01 | E-MTAB-7388 | biostudies-arrayexpress

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