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MenSCs inhibit HCC growth through oncogenic pathway suppression via regulating 5-hmC in enhancer elements [MeDIP-seq]

ABSTRACT: MenSCs inhibit HCC growth through oncogenic pathway suppression via regulating 5-hmC in enhancer elements [MeDIP-seq]

PROVIDER: PRJNA491735 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7874040.fastq.gz	Fastqsanger.gz
	SRR7874041.fastq.gz	Fastqsanger.gz
	SRR7874042.fastq.gz	Fastqsanger.gz
	SRR7874043.fastq.gz	Fastqsanger.gz
	SRR7874034.fastq.gz	Fastqsanger.gz

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Similar Datasets

MenSCs inhibit HCC growth through oncogenic pathway suppression via regulating 5-hmC in enhancer elements [MeDIP-seq]

Project description:We utilize MeDIP-seq, hMeDIP-seq and RNA-seq technologies to explore the epigenetic alterations in HCC after MenSC therapy. We provide distinct epigenetic landscapes of HCC cells mediated by MenSCs and demonstrate that MenSCs exert anticancer functions by regulating 5-hmC and 5-mC abundance in enhancer and promoter regions of oncogenic pathways. Deactivation of PI3K/AKT and RAF/ERK signaling attenuated the inhibition of FOXO3 and promoted downstream apoptosis. Moreover, an increase in PTEN further strengthened the suppressive effect on PI3K/AKT. Additionally, inactivation of phosphorylated ERK repressed c-myc-mediated EMT. Taken together, our results provided important epigenetic evidence for clarifying the mechanism of crosstalk between cancer and MSCs in the microenvironment and screening effective epigenetic targets for future therapy strategies based on modified MSCs.

2019-06-10 | GSE120085 | GEO

MenSCs inhibit HCC growth through oncogenic pathway suppression via regulating 5-hmC in enhancer elements [RNA-seq]

2019-06-10 | GSE120158 | GEO

MenSCs inhibit HCC growth through oncogenic pathway suppression via regulating 5-hmC in enhancer elements [hMeDIP-seq]

2019-06-10 | GSE120141 | GEO

MenSCs inhibit HCC growth through oncogenic pathway suppression via regulating 5-hmC in enhancer elements

Project description:MenSCs inhibit HCC growth through oncogenic pathway suppression via regulating 5-hmC in enhancer elements

| PRJNA491745 | ENA

MenSCs inhibit HCC growth through oncogenic pathway suppression via regulating 5-hmC in enhancer elements [hMeDIP-seq]

Project description:MenSCs inhibit HCC growth through oncogenic pathway suppression via regulating 5-hmC in enhancer elements [hMeDIP-seq]

| PRJNA491734 | ENA

MenSCs inhibit HCC growth through oncogenic pathway suppression via regulating 5-hmC in enhancer elements [RNA-seq]

Project description:MenSCs inhibit HCC growth through oncogenic pathway suppression via regulating 5-hmC in enhancer elements [RNA-seq]

| PRJNA491746 | ENA

MenSCs inhibit HCC growth through oncogenic pathway suppression via regulating 5-hmC in enhancer elements

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-06-10 | GSE120160 | GEO

Protein Amount in Conditioned Medium of MenSCs

Project description:Protein microarray containing 1000 factors was used to detect protein components in the conditioned media of MenSCs. Select the protein with high expression content, and the enrichment result shows that it is related to inflammatory response, negative regulation of apoptotic process, microglial cell activation, negative regulation of TNF-α production, and innate immune response. These biological processes may partly explain the therapeutic functions of MenSCs on promoting the survival of DAergic neurons and anti-inflammation by regulating microglia polarization.

2023-04-03 | GSE228520 | GEO

RNA-seq of Multilineage differentiating stress-enduring enriched cells (MECs) derived from MenSCs

Project description:The increasing interest in multilineage differentiating stress-enduring (Muse) cells within the field of regenerative medicine is attributed to their exceptional homing capabilities, prolonged viability in adverse conditions, and enhanced three-germ-layer differentiate ability, surpassing their parent mesenchymal stem cells. Given their abundant sources, non-invasive collection procedure, and periodic availability, human menstrual blood-derived endometrium stem cells (MenSCs) have been extensively investigated as a potential resource for stem cell-based therapies. However, there is no established modality to isolate Muse cells from MenSCs and disparity in gene expression profiles between Muse cells and MenSCs remain unknown. In this study, Muse cells were isolated from MenSCs by long-time trypsin incubation method. Muse cells expressed pluripotency markers and could realize trilineage differentiation in vitro. Compared with MenSCs, Muse cells showed enhanced homing ability and superior therapeutic efficacy in animal models of acute liver injury (ALI) and intracerebral hemorrhage (ICH). Furthermore, the RNA-seq analysis offers insights into the mechanism underlying the disparity in trypsin resistance and migration ability between Muse and MenSCs cells. This research offers a significant foundation for further exploration of cell-based therapies using MenSCs-derived Muse cells in the context of various human diseases, highlighting their promising application in the field of regenerative medicine.

2024-01-01 | GSE247588 | GEO

Genome-Wide Mapping of 5-mC and 5-hmC in severely Preeclamptic Placentas.

Project description:Preeclampsia (PE) is a major contributor of maternal mortality with uncertain etiology. Recent studies suggested that epigenetic modifications, including DNA methylation, play a vital role in the development of PE. In this study, we have mapped genome-wide distribution of 5-methylcytosin (5-mC) and 5-hydroxymethylcytosine (5-hmC) using MeDIP and (h)MeDIP in the placentas from severely preeclamptic patients and normal controls. A total 194485 pooled 5-mC peaks and 138133 pooled 5-hmC peaks were identified, of which 714 5-mC peaks and 119 5-hmC peaks showed significant difference between patients and controls (>2-fold, p<0.05).To our knowledge, this is the first report of DHMRs (Differentially Hydroxy-Methylated Regions) in preeclamptic placenta. We not only confirmed the aberrant DNA methylated regions in the process of preeclampsia reported previously, but also identified unreported regions. A total of 4 selected DMRs (Differentially Methylated Regions) were also confirmed by MassARRAY EppiTYPER. Of these, PTPRN2, which had low level of 5-mC and high level of 5-hmC at gene body, was further verified to have lower methylation level at promoter regions in case group compared with controls. In conclusion, our study provided genome-wide distribution of 5-mC and 5-hmC in severe PE and normal controls, which have further clinical value for the identification of diagnostic and therapeutic markers for severe PE.

2014-12-13 | GSE63743 | GEO

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