Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA243292 | ENA |
REPOSITORIES: ENA
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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:Mouse CD4+/CD8+ thymocytes from miR-181a1/b1 KO vs WT
2019-05-14 | E-GEOD-41090 | ExpressionAtlas
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: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:To understand the molecular mechanism by which IIAEK ameliorates hepatic and intestinal cholesterol metabolism, we performed DNA microarray analysis using liver, duodenal, and jejunal samples from the control and IIAEK groups of WT or IAP KO mice. We found that 1995 transcripts were identified in the livers of WT mice [WT, Control (WC) vs. WT, IIAEK (WI)] and 3802 in IAP-KO mice [IAP-KO, Control (KOC) vs. IAP-KO, IIAEK (KOI)] ( ≥1.2 fold-change, p < 0.05). Of these, 1729 transcripts fluctuated only in the WT group (WC vs. WI) and 3536 fluctuated only in the IAP-KO group (KOC vs. KOI).
2025-03-17 | GSE290764 | GEO
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:The gene expression profiles of WT and NML-KO livers
2015-07-17 | E-GEOD-48191 | ExpressionAtlas
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: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