Project description:PyMT cells (HIF-1 wild type, WT and HIF-1 knockout, KO) were compared for differential gene expression at normoxia or after exposure to hypoxia, 0.5% oxygen for 6h
Project description:We compared the transcriptional profile of mammary tumors spontaneously developed in PyMT transgenic mice either bearing or not additional copies of the endogeneous SIRT6 gene.
Project description:To investigate the role of NR1D1 in the progression of breast cancer, mammary gland tumor tissues were obtained from 14 weeks old FVB Nr1d1+/+;PyMT and Nr1d1-/-;PyMT mice and the gene expression patterns were analyzed by RNA-seq.
Project description:Previously, lncRNA Malat1 knockout mice were generated by insertional inactivation. By crossing this line to MMTV-PyMT mammary tumor mouse model, we produced PyMT;Malat1 wild-type (WT) and PyMT;Malat1 knockout (KO). Furthermore, we generated Malat1 transgenic mice by targeting ROSA26 locus and bred them to PyMT;Malat1 knockout mice to produce Malat1-rescued PyMT;Malat1 knockout;Malat1 transgenic animals (TG). Using mammary tumors from the three groups of animals, we performed RNA-Seq analysis to identify differentially up-regulated genes in KO tumors to find novel target genes of YAP-TEAD pathway.
Project description:We labeled PyMT control cells versus PyMT-GPx2 KD with GFP in vitro and then injected into mammary fat pad of mice for incubating 45 days. We then generated single cell suspension by FACS sorting from PyMT-control, GPx2 KD. 10X Genomics was used to make cDNA library. We then sequenced the samples with Illumina high throughput sequencing.
Project description:Junction Adhesion Molecule-A (JAM-A) is present on leukocytes and platelets where it promotes cell adhesion and motility. We are interested in an interaction between JAM-A and tumor progression/metastases. To address this point, we mated JAM-A-/- mice and mouse mammary tumor model MMTV-PyMT mice which, which express polyoma middle T antigen under the control of mouse mammary tumor virus. MMTV-PyMT mice show 100% penetration of mammary tumor and highly metastases to lung. MMTV-PyMT mice without JAM-A show less primary tumor progression, therefore JAM-A enhance primary tumor progression. Then we are addressing the molecular mechanism of this phenomenon by in vivo. Furthermore, we would like to examine JAM-A deficient MMTV tumor signature. Each 3 MMTV-PyMT JAm-A+/+ (JamA+) and 3 MMTV JAM-A-/- (JamA-) mammary tumor were resected at early stages of tumor development for RNA extraction and hybridization on Affymetrix microarrays.
Project description:The goal of the experiment was to carry out a transcriptome analysis of the three main epithelial cell populations of the mouse mammary gland, the basal/myoepithelial, luminal estrogen receptor negative (ER-) and luminal estrogen receptor positive (ER+) cells, to identify cell-type specific differences in gene expression. Three replicates arrays were carried out for each of the three populations (a total of nine arrays). Each replicate was a genuine biological replicate from RNA harvested from completely independent cell preparations. Each sample was isolated from preparations of mammary epithelium derived fourth mammary fat pads of 8 * 10 week old virgin female FVB mice. Each preparation was from a pool of 10 * 20 animals (20 * 40 fat pads).
Project description:Junction Adhesion Molecule-A (JAM-A) is present on leukocytes and platelets where it promotes cell adhesion and motility. We are interested in an interaction between JAM-A and tumor progression/metastases. To address this point, we mated JAM-A-/- mice and mouse mammary tumor model MMTV-PyMT mice which, which express polyoma middle T antigen under the control of mouse mammary tumor virus. MMTV-PyMT mice show 100% penetration of mammary tumor and highly metastases to lung. MMTV-PyMT mice without JAM-A show less primary tumor progression, therefore JAM-A enhance primary tumor progression. Then we are addressing the molecular mechanism of this phenomenon by in vivo. Furthermore, we would like to examine JAM-A deficient MMTV tumor signature.
Project description:S100A10 (p11) is a plasminogen receptor that regulatess cellular plasmin generation by cancer cells. In the current study we used the MMTV-PyMT mouse breast cancer model to investigate the role of p11 in oncogenesis. Genetic deletion of p11 resulted in significantly decreased tumor onset, growth rate and spontaneous pulmonary metastatic burden in the PyMT/p11-KO mice. This phenotype was accompanied by substantial reduction in Ki67 positivity, macrophage infiltration and decreased vascular density in the primary tumors, and appearance of invasive carcinoma and pulmonary metastasis. Surprisingly, immunohistochemical analysis of wild-type MMTV-PyMT mice failed to detect p11 expression in the tumors or metastatic tumor cells and loss of p11 did not decrease plasmin generation in the PyMT tumors and cells. Furthermore, tumor cells expressing p11 displayed dramatically reduced lung metastasis when injected into p11-depleted mice, further strengthening the stromal role of p11. Transcriptome analysis of the p11-depleted tumors showed marked reduction in genes involved in breast cancer development, progression, and inflammation such as AREG, MUC1 and S100A8. The PyMT/p11-KO tumors displayed remarkable increase in inflammatory cytokines such as IL-6, IL-10 and IFN-γ. Gene expression profiling and immunohistochemistry primary breast cancer samples showed that p11 mRNA and protein was significantly higher in tumors compared to normal mammary tissue. The mRNA expression was significantly associated with poor patient prognosis and significantly elevated in high grade, triple negative tumors and tumors with high proliferative index. We used microarray to detail the global programme of gene expression underlying reduced growth/establishment of P11-KO PyMT tumours.
Project description:We report the comparison of gene expression of neutrophils in the mammary gland of PyMT and PyMT-Cxcr2-/- animals as well as the one of WT bone marrow