Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA387924 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Enhancer reprogramming promotes pancreatic cancer progression and metastasis
| PRJNA388090 | ENA
Project description:Enhancer reprogramming promotes pancreatic cancer progression and metastasis [ChIP-seq]
| PRJNA387949 | ENA
Project description:Enhancer reprogramming promotes pancreatic cancer progression and metastasis [RNA-seq]
| PRJNA388127 | ENA
Project description:Arid1a promotes tumor initiation but restrains progression and metastasis in liver cancer [ATAC-seq]
| PRJNA377340 | ENA
Project description:Pancreatic cancer's poor prognosis is caused by distal metastasis, which is associated with epigenomic changes. However, the roles of 3D epigenome in pancreatic cancer biology, especially its metastasis, remain unclear. Here we compare the 3D epigenomic and transcriptomic features among cells derived from pancreatic epithelial, primary and metastatic pancreatic cancer by integrated analysis of in situ Hi-C, ChIP-seq, ATAC-seq, and RNA-seq data. We found A/B compartments, topologically associated domains (TADs), chromatin loops changed significantly in metastatic pancreatic cancer cells, which is associated with epigenetic state alterations. Moreover, we identified upregulated genes, which are located in switched compartments, common TADs with epigenetic state changing, specific TAD boundaries, and metastasis-specific enhancer-promoter loops, are related to cancer metastasis. We also find that the transcription factors mediated specific enhancer-promoter loops formation are also associated with metastasis. Taken together, these results provide a 3D epigenomic map of pancreatic cancer metastasis, which expands our knowledge of the epigenetic mechanism of pancreatic cancer metastasis and enables a better understanding of pancreatic cancer pathobiology.
2021-08-11 | GSE149103 | GEO
Project description:We found that BAP1 (BRCA1 Associated Protein-1) shows loss of heterozygosity in over 25% of pancreatic cancer patients and functions as tumor suppressor. Conditional deletion of Bap1 in murine pancreas led to genomic instability, accumulation of DNA damage, and an inflammatory response that evolved to pancreatitis with full penetrance. Concomitant expression of oncogenic KrasG12D led to malignant transformation and development of invasive and metastatic pancreatic cancer. At the molecular level, BAP1 maintains the integrity of the exocrine pancreas by regulating genomic stability and its loss confers sensitivity to radio- and platinum-based therapies.
2020-04-14 | GSE121709 | GEO
Project description:Arid1a promotes tumor initiation but restrains progression and metastasis in liver cancer [RNA-seq]
| PRJNA377343 | ENA
Project description:Arid1a promotes tumor initiation but restrains progression and metastasis in liver cancer [ChIP-Seq]
| PRJNA398201 | ENA
Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.
| S-EPMC8784167 | biostudies-literature
Project description:Phenotypic plasticity has emerged as an important mechanism of therapy resistance in cancers, yet the underlying molecular mechanisms remain unclear. Using an established breast cancer cellular model for endocrine resistance, we show that hormone resistance is associated with enhanced phenotypic plasticity, indicated by a general downregulation of luminal/epithelial differentiation markers and upregulation of basal/mesenchymal invasive markers. Our extensive omics studies, including GRO-seq on enhancer landscapes, demonstrate that the global enhancer gain/loss reprogramming driven by the differential interactions between ER-alpha and other oncogenic transcription factors (TFs), predominantly GATA3 and AP1, profoundly alters breast cancer transcriptional programs. Our functional studies in multiple biological systems support a coordinate role of GATA3 and AP1 in enhancer reprogramming that drives phenotypic plasticity to achieve endocrine resistance or cancer invasive progression. Thus, changes in TF-TF and TF-enhancer interactions can lead to genome-wide enhancer reprogramming, resulting in transcriptional dysregulations that promote plasticity and cancer therapy-resistance progression
2019-05-24 | MSV000083857 | MassIVE