Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA374984 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5262340_1.fastq.gz | Fastqsanger.gz | |||
| SRR5262340_2.fastq.gz | Fastqsanger.gz | |||
| SRR5262341_1.fastq.gz | Fastqsanger.gz | |||
| SRR5262341_2.fastq.gz | Fastqsanger.gz | |||
| SRR5262342_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:This study reveals that the millions of satellite II (HSATII) sequences in the human genome can bind and impact distribution of epigenetic regulators, and that this goes awry in cancer. In many cancers master epigenetic factors form two-types of cancer-specific nuclear bodies, caused by locus-specific deregulation of HSATII DNA and RNA, respectively. DNA demethylation at the 1q12 mega-satellite, common in cancer, causes PRC1 aggregation into prominent Cancer-Associated Polycomb (CAP) bodies. These loci remain silent, whereas HSATII loci in regions low in PRC1 become de-repressed, reflecting imbalanced distribution of UbH2A on these and other PcG-regulated loci. Large nuclear foci of HSATII RNA form and sequester copious MeCP2 into Cancer-Associated Satellite Transcript (CAST) bodies. Hence, HSATII DNA and RNA have an exceptional capacity to “sponge” epigenetic factors into abnormal nuclear bodies in cancer. Results support a new concept that demethylation of “junk” repeats can trigger further epigenetic compromise by compartmentalizing regulatory factors within nuclear structure.
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Project description:Chromosome 1 pericentric heterochromatin rearrangements : potent drivers of nuclear architecture perturbations and gene deregulation in human B cell lymphoma Epigenetic perturbations are increasingly described in cancer cells where they are thought to contribute to deregulated gene expression and genome instability. Here, we report the first evidence, that a distinct category of chromosomal translocation observed in human tumours â those targeting 1q12 satellite DNA - can directly mediate such perturbations by promoting the formation of aberrant heterochromatic foci (aHCF). By detailed investigations of a 1q12 translocation to chromosome 2p, in a case of human B cell lymphoma, aberrant aHCF were shown to be localised to the nuclear periphery and to arise as a consequence of long range âpairingâ between the translocated 1q12 and chromosome 2 centromeric regions. Remarkably, adjacent 2p sequences showed increased levels of repressive histone modifications, including H4K20me3 and H3K9me3, and were bound by HP1. aHCF were associated to aberrant spatial localisation and deregulated expression of a novel 2p gene (GMCL1) that was found to have prognostic impact in B cell lymphoma. Thus constitutive heterochromatin rearrangements can contribute to tumourigenesis by perturbing gene expression by via long range epigenetic mechanisms. The formation of aberrant heterochromatic foci, coupled to abnormal enrichment of adjacent 2p sequences in repressive heterochromatin marks (H4K20me3, H3K9me3 and HP1), delayed replication and repositioning of the rearranged chromosome 2 to the nuclear periphery, could be associated to altered gene expression of at least those genes brought into close proximity to heterochromatin. To assess this question, global gene expression profiling was performed in the lymphoma B cells presenting the aberrant heterochromatin foci (CH1), treated or not with the histone deacetylase inhibitor, trichostatin A.
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Project description:Splicing alterations are very common in cancer and might affect disease initiation and progression. In several cancers, mutations in splicing factor genes are responsible for aberrant splicing. We show that certain aggressive cancers, such as pediatric T-cell acute lymphoblastic leukemia (T-ALL), have an alternative mechanism for aberrant splicing that involves post-translational regulation of the splicing machinery via deubiquitination. We initially demonstrated that T-ALL presents with extensive exon skipping events affecting proteasomal transcripts, cell cycle and epigenetic regulators. Performing an unbiased genetic screen study for RNA binding proteins, we showed that the serine/arginine-rich splicing factor (SRSF) proteins, controlling exon skipping are critical for T-ALL survival. In our effort to dissect mechanisms of aberrant regulation of SRSF proteins, we focused on the pro-oncogenic deubiquitinase ubiquitin-specific peptidase 7 (USP7) to show it regulates the levels of the SRSF proteins at the post-translational level via active deubiquitination. We further demonstrated that USP7 inhibitors can change the splicing landscape and block T-ALL growth. Our drug studies show that decrease of the levels of SRSF proteins splicing inhibitors sensitize cells to the clinically used splicing inhibitor H3B-8800. Driven by our molecular findings on aberrant splicing of proteasomal transcripts, we demonstrate that H3B-8800 could act synergistically with proteasome inhibitors, paving the way for new therapeutic schemes in pediatric leukemia. Collectively this study provides the proof-of-principle for regulation of splicing factors independently of mutations and via deubiquitination and suggests new therapeutic modalities and combinations in cancer.
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