Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA260915 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Identifying actionable targets through integrative analyses of GEM model and human prostate cancer profiling
| PRJNA260914 | ENA
Project description:Identifying actionable targets through integrative analyses of GEM model and human prostate cancer profiling (Illumina)
| PRJNA260908 | ENA
Project description:Here we prolife prostate cancers derived from GEM models of prostate cancer representative of human prostate cancer Total DNA was isolated from established prostate cancers in 4 GEM models of prostate cancer - PB-MYC, Pten-/-, Pten-/- p53-/-, Pten-/- Rosa26-ERG, and 3 cell lines derived from GEM models including CaP8, MYC CaP, and MPC3 and normalized to wild-type prostate of litter-mate mice of same genetic background strain
2015-02-20 | E-GEOD-61382 | biostudies-arrayexpress
Project description:Here we profile prostate cancers derived from GEM models of prostate cancer representative of human prostate cancer Total RNA was isolated from established prostate cancers in 3 GEM models of prostate cancer - PB-MYC, Pten-/-, Pten-/- p53-/-
2015-02-20 | E-GEOD-61379 | biostudies-arrayexpress
Project description:Here we prolife prostate cancers derived from GEM models of prostate cancer representative of human prostate cancer
2015-02-20 | GSE61382 | GEO
Project description:Here we profile prostate cancers derived from GEM models of prostate cancer representative of human prostate cancer
2015-02-20 | GSE61379 | GEO
Project description:Advanced prostate cancer is often associated with the emergence of more aggressive disease phenotypes, including neuroendocrine prostate cancer (NEPC), which are currently incurable. To identify drivers of aggressive prostate cancer, we conducted a Sleeping Beauty (SB) transposon mutagenesis screen based on a mouse model having conditional loss of function of Pten and Tp53 prostate (NPp53). Compared with the control mice (NPp53-SB(—)), the experimental mice (NPp53-SB(+)) develop aggressive prostate cancer phenotypes that are highly heterogeneous and highly metastasis. Most notably, a high percentage of NPp53-SB(+) prostate tumors have features of NEPC, which are conserved with human prostate cancer. To identify and prioritize drivers of NEPC in these NPp53-SB(+) tumors, we used a novel integrative approach that combines (i) genomic analyses of common insert sites (CIS) for the SB transposon, (ii) VIPER analyses of control NPp53-SB(+) prostate tumors to identify master regulators (MRs) enriched in NEPC, and (iii) comparative transcriptomic analyses with data from human prostate cancer patients followed by integrative analyses using of these data using a CINDy algorithm to identify CIS-associated genes that modulate the NEPC phenotypes. Among these the nicotinamide adenosine dinucleotide (NAD)-dependent deacetylase, sirtuin 1 (Sirt1). Loss- and gain-of-function studies in human prostate cancer cell lines showed that SIRT1 promotes NEPC, while its depletion or inhibition reduces NEPC. Overall, this integrative phenotypic and systems analyses have identified of candidate drivers of NEPC and may be generalizable to analyzing and interpreting data from analogous in vivo mutagenesis screens.
2026-04-13 | GSE271053 | GEO
Project description:Advanced prostate cancer is often associated with the emergence of more aggressive disease phenotypes, including neuroendocrine prostate cancer (NEPC), which are currently incurable. To identify drivers of aggressive prostate cancer, we conducted a Sleeping Beauty (SB) transposon mutagenesis screen based on a mouse model having conditional loss of function of Pten and Tp53 prostate (NPp53). Compared with the control mice (NPp53-SB(—)), the experimental mice (NPp53-SB(+)) develop aggressive prostate cancer phenotypes that are highly heterogeneous and highly metastasis. Most notably, a high percentage of NPp53-SB(+) prostate tumors have features of NEPC, which are conserved with human prostate cancer. To identify and prioritize drivers of NEPC in these NPp53-SB(+) tumors, we used a novel integrative approach that combines (i) genomic analyses of common insert sites (CIS) for the SB transposon, (ii) VIPER analyses of control NPp53-SB(+) prostate tumors to identify master regulators (MRs) enriched in NEPC, and (iii) comparative transcriptomic analyses with data from human prostate cancer patients followed by integrative analyses using of these data using a CINDy algorithm to identify CIS-associated genes that modulate the NEPC phenotypes. Among these the nicotinamide adenosine dinucleotide (NAD)-dependent deacetylase, sirtuin 1 (Sirt1). Loss- and gain-of-function studies in human prostate cancer cell lines showed that SIRT1 promotes NEPC, while its depletion or inhibition reduces NEPC. Overall, this integrative phenotypic and systems analyses have identified of candidate drivers of NEPC and may be generalizable to analyzing and interpreting data from analogous in vivo mutagenesis screens.
2026-04-13 | GSE271054 | GEO
Project description:Abstract Background. The cellular effects of androgen are transduced through the androgen receptor, which controls the expression of genes that regulate biosynthetic processes, cell growth, and metabolism. Androgen signaling also impacts DNA damage signaling through mechanisms involving gene expression and transcription-associated DNA damaging events. Defining the contributions of androgen signaling to DNA repair is important for understanding androgen receptor function, and it also has important translational implications. Methods. We generated RNA-seq data from multiple prostate cancer lines and used bioinformatic analyses to characterize androgen-regulated gene expression. We compared the results from cell lines with gene expression data from prostate cancer xenografts, and patient samples, to query how androgen signaling and prostate cancer progression influences the expression of DNA repair genes. We performed whole genome sequencing to help characterize the status of the DNA repair machinery in widely used prostate cancer lines. Finally, we tested a DNA repair enzyme inhibitor for effects on androgen-dependent transcription. Results. Our data indicates that androgen signaling regulates a subset of DNA repair genes that are largely specific to the respective model system and disease state. We identified deleterious mutations in the DNA repair genes RAD50 and CHEK2. We found that inhibition of the DNA repair enzyme MRE11 with the small molecule mirin inhibits androgen-dependent transcription and growth of prostate cancer cells. Conclusions. Our data supports the view that crosstalk between androgen signaling and DNA repair occurs at multiple levels, and that DNA repair enzymes in addition to PARPs, could be actionable targets in prostate cancer.
2018-09-30 | GSE120660 | GEO
Project description:Integrative epigenomic analyses of HGSOC model cells
| PRJDB14752 | ENA