Project description:Gene expression profiling of disseminated tumor cells in lung, lung metastatses and residual tumor cells in the MMTV-PyMT breast cancer model. Profiling gene expression change between disseminated tumor cells, lung metastases and residual tumor cells from the MMTV-PyMT breast cancer model.
Project description:Gene expression profiling of disseminated tumor cells in lung, lung metastatses and residual tumor cells in the MMTV-PyMT breast cancer model.
Project description:We aimed to understand the transcriptome patterns of organ-derived cancer cell isolates from MMTV-PyMT mice. Tissues from primary tumors and organs harboring distal metastases were harvested from cancer bearing female mice. Although metastatic progression from primary tumors to lung tissue is well studied in the MMTV-PyMT model, metastases to other distal organs and the significance of intratumor heterogeneity across metastases from distal organs remain unclear. To gain insight, we established an array of metastatic cell lines harvested from the MMTV-PyMT breast cancer mouse model. Sequencing at bulk and single-cell level were performed and used to examine the effects of cell heterogeneity on metastases and organ tropism
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: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:In order to identify transciptomic changes of endothelial cells (Ecs) in response to STING activation, endothelial cells were soted using FACS and RNA-seq was performed. We compared ECs from 3 models; normal mammary fat pad, MMTV-PyMT spontaneous breast tumor, implanted breast tumor. Tumor cells derived from MMTV-PyMT spontaneous breast tumor were expanded on culture and implanted in mammary fat pad of female FVB mice to establish implanted breast tumor model.
Project description:In this study, radiation therapy was performed on mouse breast cancer spontaneous gene mice (MMTV-PyMT) to obtain radiation therapy model of breast cancer mice. To simulate clinical breast cancer radiotherapy and study the differential proteins of breast cancer radiotherapy resistance. MMTV-PyMT mice were randomly divided into two groups, and the radiotherapy group was given the same dose 5 times (3GY, once every 2 days) when the breast cancer tumor grew to an appropriate size (200mm3). The protein extracted from mouse tumor was analyzed by mass spectrometry.
Project description:MicroRNAs (miRNAs) are small noncoding RNAs that typically inhibit the translation and stability of messenger RNAs (mRNAs), controlling genes involved in a variety of cellular processes. miRNA dysregulation is recognized to play an essential role in the development and progression of cancer. MMTV-PyMT mice (Jax Strain: FVB/N-Tg(MMTV-PyVT)634Mul/J) are a well-characterized transgenic mouse model of breast cancer. Upon activation of the MMTV-PyVT transgene (mouse mammary tumor virus (MMTV) long terminal repeat upstream of a cDNA sequence encoding the Polyoma Virus middle T antigen (PyVT)) female carriers develop palpable mammary tumors as early as 5 weeks of age. We performed miRNA microarrays on samples from the MMTV-PyMT transgenic mouse model to investigate the differential expression of miRNAs during development of malignant disease in this model.
Project description:Here, we use single cell sequencing to delineate the heterogeneity of tumours from the genetically engineered MMTV-PyMT mouse model of breast cancer (MMTV-PyMT::K14Cre::Rosa-tdTomato mice).
Project description:Breast carcinoma cell invasion is thought to depend on the mobilization of the membrane-anchored matrix metalloproteinase, Mmp14/MT1-MMP, to drive the remodeling of extracellular matrix and trigger associated signaling cascades. However, the roles that this proteinase plays during breast tumor progression and invasion in vivo remain undefined. A highly penetrant syngeneic mouse model for luminal B breast cancer driven by the polyoma middle T (PyMT) antigen, in tandem with recently developed Mmp14-floxed mice and MMTV-Cre transgenics that express Cre recombinase throughout the mammary epithelial cell compartment, were used to characterize the impact of conditional Mmp14-targeting on breast carcinoma cell invasion programs in vivo. Transcriptome profiling of intact MMTV-PyMT carcinoma tumors was used to investigate the functional roles of carcinoma cell-derived MT1-MMP in MMTV-PyMT tumor progression and invasion in an unbiased fashion
