Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA407072 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6031970_1.fastq.gz | Fastqsanger.gz | |||
| SRR6031970_2.fastq.gz | Fastqsanger.gz | |||
| SRR6031971_1.fastq.gz | Fastqsanger.gz | |||
| SRR6031971_2.fastq.gz | Fastqsanger.gz | |||
| SRR6031972_1.fastq.gz | Fastqsanger.gz |
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Project description:A Suv39H1-low chromatin state drives migratory cell populations in cervical cancer
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Project description:The evolution of migratory populations of cells within solid tumours represents a critical stage during cancer metastasis. We have previously reported the enhanced migratory properties of one such population, marked by the expression of CD66, within cervical cancers. However, it is not clear what mechanisms drive such migratory populations, and how these cells would retain a “memory” of initial migration-inducing cues during metastasis. Here, we describe the role of a Suv39H1-low heterochromatin state as a driver of cervical cancer migratory populations. Cervical cancer cells were sorted based on migratory ability in vitro. These migrated populations show low Suv39H1, and Suv39H1 knockdown enhances cell migration. Using histopathology to examine clinical carcinoma progression, initial progression showed expansion of a proliferative Suv39H1high population, followed by the emergence of a sarcomatoid, migratory Suv39H1low cell population in advanced stages. Additionally, meta-analysis of TCGA data revealed that low tumoural Suv39H1 also correlated with lower patient survival, and with expression signatures of migration, TGF-β signalling, and links with a CD66 cell signature. Lastly, using RNA-Seq and H3K9me3 ChIP-Seq on migrated populations in vitro, it was observed that these populations show Suv39H1-linked transcriptome alterations and broad scale H3K9me3 remodelling. This Suv39H1-linked heterochromatin regulation could explain plasticity in migratory and metastatic populations, and allows for a “memory” of migration inducing cues, through metastable changes in chromatin conformation. The understanding of such regulatory mechanisms in migratory populations may prove valuable in efforts to develop anti-metastatic strategies.
2019-03-01 | GSE103793 | GEO
Project description:The evolution of migratory populations of cells within solid tumours represents a critical stage during cancer metastasis. We have previously reported the enhanced migratory properties of one such population, marked by the expression of CD66, within cervical cancers. However, it is not clear what mechanisms drive such migratory populations, and how these cells would retain a “memory” of initial migration-inducing cues during metastasis. Here, we describe the role of a Suv39H1-low heterochromatin state as a driver of cervical cancer migratory populations. Cervical cancer cells were sorted based on migratory ability in vitro. These migrated populations show low Suv39H1, and Suv39H1 knockdown enhances cell migration. Using histopathology to examine clinical carcinoma progression, initial progression showed expansion of a proliferative Suv39H1high population, followed by the emergence of a sarcomatoid, migratory Suv39H1low cell population in advanced stages. Additionally, meta-analysis of TCGA data revealed that low tumoural Suv39H1 also correlated with lower patient survival, and with expression signatures of migration, TGF-β signalling, and links with a CD66 cell signature. Lastly, using RNA-Seq and H3K9me3 ChIP-Seq on migrated populations in vitro, it was observed that these populations show Suv39H1-linked transcriptome alterations and broad scale H3K9me3 remodelling. This Suv39H1-linked heterochromatin regulation could explain plasticity in migratory and metastatic populations, and allows for a “memory” of migration inducing cues, through metastable changes in chromatin conformation. The understanding of such regulatory mechanisms in migratory populations may prove valuable in efforts to develop anti-metastatic strategies.
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Project description:A Suv39H1-low chromatin state drives migratory cell populations in cervical cancer [RNA-Seq]
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Project description:We assembled a quantitative map for the abundance and interactions of 16 factors related to PCH in living cells and found that stably bound complexes of the histone methyltransferase Suv39h1/2 demarcate the PCH state. From the experimental data we developed a predictive mathematical model that explains how chromatin-bound Suv39h1/2 complexes act as nucleation sites and propagate a spatially confined PCH domain with elevated histone H3 trimethylation levels via chromatin dynamics. Enrichment of HP1, Suv39h1/h2, H3K9me3 and H3K36me3 was assessed by ChIP-seq in NPCs derived from ESCs showing differential occupation at intergenic major satellite repeats and enrichment of heterochromatin factors. ChIP-seq of HP1, Suv39h1, Suv39h2, H3K9me3, H3K36me3 in NPCs
2014-08-12 | E-GEOD-58555 | biostudies-arrayexpress
Project description:We assembled a quantitative map for the abundance and interactions of 16 factors related to PCH in living cells and found that stably bound complexes of the histone methyltransferase Suv39h1/2 demarcate the PCH state. From the experimental data we developed a predictive mathematical model that explains how chromatin-bound Suv39h1/2 complexes act as nucleation sites and propagate a spatially confined PCH domain with elevated histone H3 trimethylation levels via chromatin dynamics. Enrichment of HP1, Suv39h1/h2, H3K9me3 and H3K36me3 was assessed by ChIP-seq in NPCs derived from ESCs showing differential occupation at intergenic major satellite repeats and enrichment of heterochromatin factors.
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Project description:Skin draining lymph node dendritic cell populations are known to be diverse and distinguishable via their migratory or resident properties as well as by lineage. We analyzed these populations at steady state and during the sensitization phase of the Th2-driven FITC-hapten contact hypersensitivity (CHS) model. We also analyzed the dendritic cells populations of CLEC4C-DTR+ mice treated with diptheria toxin, which demonstrate exacerbated pathology in the FITC-CHS model. We demonstrate the diversity of dendritic cell populations at steady state and during type 2 inflammation, and surprisingly, reveal a skewing of the DC populations in DT treated CLEC4C-DTR+ mice, with an enrichment of DC2 migratory populations and depletion of CD326+ migratory cells in addition to pDC.
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Project description:Prior investigations have delineated the multifarious roles of EGFL7 within various cancer contexts. Nevertheless, the precise involvement of EGFL7 in the realm of human cervical carcinoma remains unclear. In this study, we investigated the relationship between EGFL7 polymorphisms and cervical cancer susceptibility in the Han Chinese population. Concurrently, we have scrutinized the expression patterns of EGFL7 in both the neoplastic cervical tissues and the cell lines HeLa and C33A. Furthermore, we explored the potential biological functions that EGFL7 may assume in the tumorigenesis of cervical cancer. Our findings manifest that the single nucleotide polymorphism rs9411260, ensconced within the transcriptional regulatory domain of EGFL7, is associated with cervical cancer risk in a Han Chinese population. Additionally, the mRNA expression of EGFL7 within cervical carcinoma tissues and the HeLa and C33A cell lines exhibits a marked reduction when compared with their adjacent normal counterparts and ECT1/E6E7 cells. Manipulation of EGFL7 expression precipitates alterations in the adhesion and migratory ability of cervical cancer cells. This investigation endows us with novel insights into the pathogenesis of cervical cancer.
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Project description:Comparable plasma lipid changes in patients with high-grade cervical intraepithelial neoplasia and patients with cervical cancer
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Project description:The study examined the infection state of HPV in the Uyghur population with cervical cancer, followed by genotyping to determine the variation in the types of HPV. Using microRNA microarray technology, differential gene expression between HPV-infected cervical cancer and uninfected normal cervical tissues was determined. The microarray results were verified by qRT-PCR using 20 sets of HPV-infected cervical cancer and uninfected cervical tissues.
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