RNA-seq of PCNA WT/PyMT mammary tumor cell and PCNA 211F mammary tumor cell
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE150513 | GEO | 2021/08/24
REPOSITORIES: GEO
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Project description:RNA-seq of PCNA WT/PyMT mammary tumor cell and PCNA 211F mammary tumor cell
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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.
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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.
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Project description:Generating a new mouse model for breast cancer heterogenaity. We use lentiviral infection to integrate the sporatically transforming EF1α-PyMT10C or Muc-PyMT10C into mouse mammary epithelial cell genomes. We then transplant those cells into cleared mammary fat pads of recipient mice, allowing tumors to develop from luminal , myoepithelial, stem and progenitor cell lineages. We developed a wide variety of tumors including rare histologies such as squamous, tubular, spindloid and lipid rich. We used microarray analysis to compare our mouse model with a microarray analysis of 9 established mouse models (Herschkowitz, J.I. et al. Genome Biology, 2007). Heirarchal clustering was used to establish the molecular subtype of tumors developed through the lentiviral-PyMT mouse model. In addition, micrarray analysis was used in conjunction with GeneSifter and GO ontology to identify unique pathways for each of the rare tumor types 43 total microarrays were generated from lentiviral-PyMT tumors, MMTV-PyMT transgenic tumors, and embryonic samples . Nine samples were two color arrays run at UNC microarray facility, while 34 were one color arrays run at Huntsman Cancer Instutite. The two color arrays were treated as one color arrays, we used the Cy3 intensity data for analysis. These data were merged and normalized (quantile and combat) with previously published arrays from UNC. Data were filtered on an intrinsic gene set developed in 2007 (Herschkowitz, J.I. et al. Genome Biology, 2007) and clustered using euclidian distance metrics This GEO submission consists of the 34 one color arrays run at Huntsman Cancer Instutite. The nine two color arrays run at UNC microarray facility are not included.
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Project description:Single cell RNA sequencing on PyMT mammary gland tumor cells
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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.
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Project description:CRISPR Cas9-based functional genomics screening is a powerful approach for identifying and characterizing novel oncology drug targets. Here, we elucidate the synthetic lethal mechanism of deubiquitinating enzyme USP1 in cancers with underlying DNA damage vulnerabilities, specifically BRCA1/2 mutant tumors and a subset of BRCA1/2 wild-type (WT) tumors. In sensitive cells, pharmacological inhibition of USP1 leads to decreased DNA synthesis concomitant with the induction of S-phase-specific DNA damage. Genome-wide CRISPR-Cas9 screens identified RAD18 and UBE2K, which promote PCNA mono- and polyubiquitination respectively, as downstream mediators of USP1 dependency. The accumulation of mono- and polyubiquitinated PCNA following USP1 inhibition was associated with a reduction in total PCNA protein levels. Ectopic expression of WT and ubiquitin-dead K164R PCNA reversed USP1 inhibitor sensitivity. Our results demonstrate, for the first time, that USP1 dependency hinges on the aberrant processing of mono- and polyubiquitinated PCNA. Moreover, this mechanism of USP1 dependency extends beyond BRCA1/2 mutant tumors to a novel subset of BRCA1/2 WT cancer enriched in ovarian and lung lineages. We further show PARP and USP1 inhibition are strongly synergistic in BRCA1/2 mutant cell lines and xenograft models. We postulate USP1 dependency unveils a previously uncharacterized vulnerability linked to post-translational modifications of PCNA. Taken together, USP1 inhibition may represent a unique therapeutic strategy for BRCA1/2 mutant tumors and a subset of BRCA1/2 WT tumors.
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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.
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Project description:Cells expressing phosphorylation-mimicking PCNA, PCNA-Y211D, show elevated hallmarks specific to the epithelial-mesenchymal transition (EMT), including the upregulation of EMT-promoting factor Snail and the downregulation of EMT-inhibitory factors E-cadherin and GSK3β. These cells exhibit active cell migration and also undergo G2/M arrest. Interestingly, all of these EMT-associated activities require the activation of ATM and Akt, as inactivating these protein kinases by gene knockdown or inhibitors blocks EMT-associated signaling and cell migration. We conclude that PCNA phosphorylation promotes cancer progression via the ATM/Akt/GSK3β/Snail signaling pathway. This study, therefore, identifies a novel PCNA function and provides the molecular basis of phosphorylated PCNA-mediated cancer development and progression.
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