Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA243292 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Previously we have demonstrated that inactivation of retinoic acid receptor beta (Rarb) in the mouse results in a protective effect against ErbB2-induced mammary gland tumorigenesis although Rarb has been reported as a tumor suppressor before. In the current study, we further confirmed that ablation of Rarb has a very similar impact on Wnt1-induced mammary gland tumorigenesis as those on ErbB2-induced mammary gland tumorigenesis. Nevertheless, the mechanisms by which Rarb confers its effects on tumor progression is quite different although both involving in tumor microenvironment (TME) remodeling. In the Wnt1 tumors, ectopic wnt1 produced by malignant luminal cells activates nearby stromal cells by a paracrine manner. In return, the stromal cells secreted IGF1 to regulate the growth of tumor cells. There is a need of Rarb expression in this interaction. Deletion of Rarb inhibits both wnt1/β-catenin signaling and IGF1/Akt axis in the myoepithelial tumor cells which results in the suppression of epithelial-mesenchymal transition (EMT) in these tumors. Since wnt1 tumors resemble basal-like breast cancer with a poor clinical prognosis in which EMT is one of the most important way for tumor cells to survive against standard treatment and to go to metastasis, we propose that (1) the stromal gene expression signature of Rarb ablation in wnt1 tumors could have some clinical value in predicting the breast cancer outcome; and (2) Rarb antagonist might be a potential therapeutic strategy in EMT-driven aggressive cancers such as basal-like breast cancer. Laser capture microdissection (LCM) was performed to separate the mammary tumor samples into epithelial cell compartment and stromal cell compartment. Transcriptional profiling of the two compartments were investigated by microarray analysis.
2014-10-23 | E-GEOD-56391 | biostudies-arrayexpress
Project description:Previously we have demonstrated that inactivation of retinoic acid receptor beta (Rarb) in the mouse results in a protective effect against ErbB2-induced mammary gland tumorigenesis although Rarb has been reported as a tumor suppressor before. In the current study, we further confirmed that ablation of Rarb has a very similar impact on Wnt1-induced mammary gland tumorigenesis as those on ErbB2-induced mammary gland tumorigenesis. Nevertheless, the mechanisms by which Rarb confers its effects on tumor progression is quite different although both involving in tumor microenvironment (TME) remodeling. In the Wnt1 tumors, ectopic wnt1 produced by malignant luminal cells activates nearby stromal cells by a paracrine manner. In return, the stromal cells secreted IGF1 to regulate the growth of tumor cells. There is a need of Rarb expression in this interaction. Deletion of Rarb inhibits both wnt1/β-catenin signaling and IGF1/Akt axis in the myoepithelial tumor cells which results in the suppression of epithelial-mesenchymal transition (EMT) in these tumors. Since wnt1 tumors resemble basal-like breast cancer with a poor clinical prognosis in which EMT is one of the most important way for tumor cells to survive against standard treatment and to go to metastasis, we propose that (1) the stromal gene expression signature of Rarb ablation in wnt1 tumors could have some clinical value in predicting the breast cancer outcome; and (2) Rarb antagonist might be a potential therapeutic strategy in EMT-driven aggressive cancers such as basal-like breast cancer.
2014-10-23 | GSE56391 | GEO
Project description:Inactivation of RAR-b, which has been reported as a tumor suppressing gene by numerous studies, results in protective effect against the tumorigenesis induced by activated ErbB2. Moreover, tissue recombination indicates that the RAR-b deficient-microenvironment, rather than the RAR-b status of mammary epithelial cells, plays a key-determining role in the initiation and progression of the mammary carcinoma. Ablation of RAR-b extensively modulates the remodeling of stroma during tumor progression through suppressing the activation and transdifferetiation of myofibroblasts. RNA microarray has been employed to identify the gene expression signature in the mammary stroma of our RAR-b null animals. We want to find out the underlining mechanism of the protective effects resulted from Rarb abliton. A global gene expression profile of mouse mammary stroma was obtained on total RNA from the cleared mammary fat pads (stroma) of both RAR-b KO (n=3) and their wild type (n=3) littermates at the age of four weeks.
2010-12-18 | E-GEOD-19925 | biostudies-arrayexpress
Project description:The goal of the experiment was to demonstrate if the overexpression of human-Prune-1 in Triple Negative breast cancer cells induces M2-polarization of macrophages in vitro. For this purpose, murine primary cells from breast tumor developed by Genetically Engineered Mouse Models (GEMMs) of TNBC (i.e., MMTV-Wnt1) and metastatic TNBC overexpressing both human Prune-1 and Wnt1 in mammary gland (i.e., MMTV-Prune-1/Wnt1) were obtained. Conditioned media were collected from these primary cells (1x106 cells) after 24 hours. Murine macrophages (J774A.1 and Raw264.7; 1x106) were starved for six hours and then grown for 48 hours in those conditioned media collected from MMTV-Wnt1 and MMTV-Prune-1/Wnt1 cells. Untreated macrophages were used as negative control for the experiment.
2020-12-03 | E-MTAB-9231 | biostudies-arrayexpress
Project description:The transcriptome of WT and Rarb KO hematopoietic stem cells (HSC) after 24h in vitro culture upon retinoid treatment was assessed by RNAseq.
2021-11-02 | E-MTAB-9749 | biostudies-arrayexpress
Project description:The purpose is to study DMBA-induced transcriptome in WT and in Cip2a-/- mouse mammary gland tissues. We identified differentially expressed genes in DMBA-induced mammary gland in WT vs. Cip2a-/- mouse mammary glands.
2021-04-28 | GSE173405 | GEO
Project description:Purpose: The goals of this study are to compare mammary tumor transcriptome profiling with or without DDR1 in immunocompetent mice in an unbiased way. Methods: In vitro samples: DDR1 WT or KO in vitro cultured E0771 cells were sequenced. Rag1-/- samples: DDR1 WT or KO E0771 cells were injected in Rag1-/- mice, and tumors were harvested and sequenced. C57BL/6 samples: DDR1 WT or KO E0771 cells were firstly inoculated into Rag1-/- mice. When tumor volume reached approximately 200~300 mm3 (usually 20 days after inoculation), 60 mg of tumor organoid were transplanted to WT C57BL/6 mice. Tumor samples were collected on day 4 after transplantation for RNA-seq. Antibody treatment samples: DDR1 KO E0771 cells were reconstituted with human DDR1, then injected into C57BL/6 mice. Isotype control IgG or anti-hDDR1 ECD antibody treatment (10mg/kg intrutumural) started when tumor volume reached approximately 100 mm3. Tumor samples were collected on day 6 after treatment for RNA-seq. Results: Approximately 50 million sequence reads were obtained per sample and identified more than 20,000 transcript isoforms. Conclusions: The RNA-seq results represents the detailed analysis of DDR1 WT/KO mammary tumor transcriptomes in immunocompetent mice C57BL/6.
2021-09-07 | GSE139239 | GEO
Project description:Variant analysis from whole exome sequencing (WES), performed on primary tumorigenic cells obtained from (1) a GEMM of metastatic TNBC mice model overexpressing both human Prune-1 and Wnt1 under the control of Mouse Mammary Tumor Virus MMTV promoter in mammary gland (i.e., MMTV-Prune-1/Wnt1); (2) a GEMM of TNBC mice model overexpressing Wnt1 under the control of MMTV promoter in mammary gland (i.e., MMTV-Wnt1).
2020-12-03 | PRJEB41714 | EVA
Project description:control vs doxorubicin treated mESC WT, p53 KO mESC, and Dux KO mESC
2021-05-21 | GSE149232 | GEO
Project description:Therapeutic targeting MTDH-SND1 interaction Suppresses Breast Cancer Progression and Metastasis (GSE159764). To further elucidate the tumor intrinsic effects of the targeting and the adverse effects on normal mammary epithelial cells Mouse mammary tumor cells and normal mammary epithelial cells were isolated from transgenic mouse models and cultured in vitro 3D spheroids system. MMTV-PyMT tumor cells from cKO mouse in tumorsphere culture were treaed with tamoxifen to induce Mtdh KO, and compared to the mock treatment which maintain wild type Mtdh. Thus the tumor intrinsic effects can be determined Normal mammary epithelial cells were isolated from mouse mammary gland and cultured in vitro in mammosphere. The cells were treated with inhibitor C26A6 vs control and thus the adverse effects on normal MECs can be determined.
2021-09-07 | GSE174622 | GEO