ATAC-seq analysis of radioresistant/sensitive cells in oral cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE180074 | GEO | 2022/01/01
REPOSITORIES: GEO
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Project description:Background: Growth hormone-secreting pituitary adenoma (GHPA) is an insidious disease with persistent hypersecretion of growth hormone and insulin-like growth factor 1, leading to increased morbidity and mortality. Though treatments for GHPA have greatly improved, lack of deep knowledge on the precise molecular mechanisms involved in GHPA hinders the development of therapeutic approaches. Few studies have attempted to reveal the genome-wide landscape of GHPA. As chromatin structure change exerts significant influence on gene transcription, herein, we investigated the landscape of chromatin accessibility. Methods: Both assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) and RNA sequencing (RNA-seq) were applied to identify the differential expression genes (DEGs) and uncover chromatin accessibility changes and the potentially associated transcription factor (TFs) in somatotropinoma tissues. Results: 64 DEGs were obtained, including 10 DEGs were elevated in the tumors and 54 DEGs were negligibly expressed in adenomas. A total of 3916 increased and 2895 decreased chromatin-accessible regions were identified nearby these DEGs. The majority of DEGs associated with closed chromatin regions were significantly down-regulated in our study, while the most of DEGs near open chromatin were not expectantly up-regulated. Additionally, the newly opened and closed chromatin regions were highly enriched for GRE and CTCF transcription factor binding sites, which were potentially relevant to the regulation of chromatin accessibility and genes expression in GHPA. Conclusion: Collectively, our results reveal the landscape of chromatin accessibility and unique enhancer in GHPA, which may, at least in part, contribute to tumorigenesis and provide a new field of drug development.
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Project description:Adult hematopoietic stem cells (HSCs) react to various stress conditions by rapidly proliferating and preferentially differentiating towards desired cell types. However, it is unclear whether and how HSCs respond to severe anemic conditions. Here we demonstrate that HSCs rapidly proliferate and enhance their erythroid potential upon induction of acute anemia. Under severe anemic conditions, the concentration of erythropoietin (EPO) does not increase in the bone marrow. Instead, lipoprotein profiles largely changed, and the concentration of apolipoprotein E (ApoE) increased. In HSCs, transcription levels of lipid metabolism-related genes such as very low-density lipoprotein receptor (Vldlr) were significantly up-regulated. Stimulation of HSCs with recombinant ApoE enhanced the erythroid potential, while HSCs of ApoE knockout mice did not respond to the hemolysis induction. We also found that VLDLRhighHSCs have higher erythroid differentiation potential, particularly after acute anemia induction. VLDLRhighHSCs were epigenetically distinct from VLDLRlowHSCs, as their chromatin accessibility was lower and more chromatin regions were closed upon acute anemia induction. Finally, we identified that the chromatin regions closed upon the acute anemia induction were mainly binding sites of a transcription factor Erg. Treatment of HSC with Erg inhibitor enhanced erythroid differentiation potential, as seen in the ApoE treatment. Our findings indicate that lipoprotein metabolism, particularly ApoE, plays a crucial role in HSC regulation under severe anemia conditions in a non-canonical fashion, unlike a conventional factor such as EPO.
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Project description:Purpose: Evaluate changes in chromatin accessibility between human embryonic stem cells and surface ectoderm cells with and without the transcription factor p63. Method: Chromatin accessibility profiles for human embryonic stem cells and surface ectoderm with and without p63 were generated by deep sequencing, in duplicate, with the Illumina NextSeq sequencer. Quality reads were assessed by fastq. Reads were aligned using Bowtie2, PCR duplicates and mitochondrial DNA were discarded, and peak calling was completed using MACS2. Non-reproducible peaks were filtered out by IDR with an FDR of 5%. Results: p63 fails to modify chromatin accessibility when ectopically expressed in human embryonic stem cells; differentiation of human embryonic stem cells to surface ectoderm results in the closure of some regions open in pluripotent cells and the opening of new regions; and loss of p63 in the surface ectoderm results in increased accessibility of 1/3 of the regions opened during surface ectoderm differentiation. Conclusion: p63's ability to modify chromatin accessibility is dependent upon the underlying epigenetic landscape, and when it can modify the landscape, it does so by closing regions that become open during ectoderm differentiation.
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Project description:Escherichia coli strain:1929 | isolate:1929 Genome sequencing
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