ABSTRACT: Stem cell gene expression profiling of primary mammary tumors derived from orthotopic xenograft tumors treated with Sulforaphane (SFN) or control I
Project description:Stem cell gene expression profiling of primary mammary tumors derived from orthotopic xenograft tumors treated with Sulforaphane (SFN) or control
Project description:Stem cell gene expression profiling of primary mammary tumors derived from orthotopic xenograft tumors treated with Sulforaphane (SFN) or control II
Project description:In this study, we explored stem cell markers profile of mammary tumor initiation and growth derived from a human breast cancer cell line (MDA-MB-231 D3H1 Luci). In this dataset, we include expression data from primary mammary tumors pre-treated with Sulforaphane for 2 weeks (daily i.p. injection of 50mg SFN/kg) and kept treatment after cell injection for more 3 weeks and Saline 0.9% as a Control.
Project description:In this study, we explored stem cell markers profile of mammary tumor initiation and growth derived from a human breast cancer cell line (MDA-MB-231 D3H1 Luci). In this dataset, we include expression data from primary mammary tumors pre-treated with Sulforaphane for 2 weeks (daily i.p. injection of 50mg SFN/kg) and kept treatment after cell injection for more 3 weeks and Saline 0.9% as a Control.
Project description:cMET is a well known oncogene whose activation is widely implicated in tumorigenesis and metastasis. To investigate the effects of acute inhibitoin of cMET signaling in the mammary tumors, we inhibited cMET activation in xenograft mammary tumors that were derived from a MET amplified mouse mammary tumor cell line and analyzed the transcriptional alteration between vehicle and MET inhibitor treated tumors.
Project description:RNA-sequencing analysis of control and SMYD3-knockdown MDA-MB-231 tumors from the mammary glands of orthotopic xenograft NOD/SCID mice. SMYD3 (also known as KMT3E), a hisone H3 lysine K4 methyltransferase, is highly expressed in several human cancers, including colorectal and breast carcinomas. Results provide insight into the transcriptional regulation of SMYD3 in breast cancer.
Project description:Analysis of ferroptosis markers from cells isolated from neuroblastoma orthotopic xenograft mouse model. We combine simultaneous inhibition of cysteine uptake and transsulfuration in xenograft model using SK-N-DZ cell line. We treated the mice with IKE and PPG together with genetic targeting of GPX4 activity. At the end of the treatment, transcriptional profiling of residual small tumors revealed induction of ferroptosis markers after combined inhibition of cystine uptake/cysteine synthesis and GPX4 as compared to tumors treated with vehicle control.
Project description:To investigate the impact of combined Rb and p53 loss in mammary tumorigenesis, we used transgenic and viral approaches to delete Rb and p53 floxed alleles specifically in the mouse mammary epithelium. Although MMTV-Cre (NLST) targets stem/bi-potent progenitors in the mammary gland, a subset of MMTV-Cre:Rbf/f;p53f/f mice developed non-mammary tumors. Thus, freshly isolated primary mammary epithelial cells from these animals were transplanted into the mammary fat pads of immunodeficient mice and monitored for tumor formation. In addition, primary MECs were isolated from Cre-negative Rbf/f;p53f/f mice, infected with Ad-Cre followed by orthotopic transplantation. In all these cases, resulting tumors shared similar spindle-shape histology, expressed high levels of vimentin, a mesenchymal marker, but not E-cadherin, a luminal marker, and were classified as adeno-sacrcomatoid/spindle-cell/mesenchymal-like breast cancer. We used microarrays to detect differentially expressed genes in the Rb/p53 double-knock-out vs p53 single deletion or normal mammary tissue. Total RNA was extracted from tumors developed by double Trizol method and hybridized on Affymetrix microarrays
Project description:Using the orthotopic breast cancer xenograft model of basal-like breast cancer MDA-MB-231 line, we have found that the expression of miRNAs encoded by MIR17HG was significantly decreased in cells isolated from spontaneous lung metastases compared to cells from primary tumors grown in orthotopic sites. We investigated the role of a MIR17HG family member, miR-18a, in primary tumor growth and pulmonary metastasis from the orthotopic site. We demonstrated that enforced expression of exogenous miR-18a, significantly limited continuous growth of primary tumors in mammary gland fat pads and reduced spontaneous lung metastasis. Further investigation on the mechanism of miR-18a action led to the finding that the expression of HIF1A, a key regulator of tumor metastasis, was regulated by miR-18a. Enforced miR-18a expression significantly decreased HIF1A expression at both mRNA and protein levels, resulting in altered transcriptional response and decreased survival of cells in response to Cobalt(II) chloride (CoCl2), a hypoxia-mimicking agent. Conversely, miR-18a knockdown significantly increased HIF1A expression levels and enhanced cell survival in response to CoCl2. Analysis of expression data of human breast tumor tissues showed that miR-18a expression is inversely correlated with HIF1A expression in basal-like breast tumors, supporting a role of miR-18a in restricting HIF1A expression in this subtype of breast cancer. In addition, we demonstrated that hypoxia inhibits miR-18a expression, likely through MYC inactivation. Furthermore, gene expression and functional analysis revealed that miR-18a also plays a role in regulating cell adhesion, migration and invasion. Taken together, this study provides evidence for a novel role of miR-18a to inhibit breast cancer metastasis. Our results suggest that miR-18a downregulation might provide tumor cells survival/growth advantage under hypoxic pressure in basal-like breast cancer. A lung metastatic subline, designated as MB231RN-LM, was derived from MDA-MB-231 breast cancer cells through in vivo selection. The MB231RN-LM cells were stably transfected with has-miR-18a or control vector and treated with 200uM Cobalt(II) chloride (CoCl2, a hypoxia-mimicking agent) for 4 hr. A total of 8 samples were subjected to microarray analysis, with two biological repeats for each experiment condition.
Project description:We kept a primary xenograft models (KURC;Kyoto University Renal Cancer-3) derived from human renal cell carcinoma tissues, and 10 mg/kg of temsirolimus or vehicle was intraperitoneally administered.We performed DNA methylation analysis to compare the methylation profile of temsirolimus-treated primary xenograft tumors with that of vehicle-treated.