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

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

PROVIDER: PRJNA491746 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7874130.fastq.gz	Fastqsanger.gz
	SRR7874131.fastq.gz	Fastqsanger.gz
	SRR7874122.fastq.gz	Fastqsanger.gz
	SRR7874132.fastq.gz	Fastqsanger.gz
	SRR7874123.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 [RNA-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 | 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 [MeDIP-seq]

2019-06-10 | GSE120085 | 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 [MeDIP-seq]

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

| PRJNA491735 | 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

Comprehensive mapping of 5-hmC epigenetic dynamics in axon regeneration

Project description:In contrast to CNS neurons, dorsal root ganglia (DRG) neurons can switch to a regenerative state after peripheral axotomy. In a screen for chromatin regulators of the regenerative responses in this conditioning lesion paradigm, we identified Tet methylcytosine dioxygenase 3 (Tet3) as upregulated, along with increased 5-hydroxymethylcytosine (5-hmC) in DRG neurons. We generated genome-wide 5-hmC maps in adult DRG, which demonstrated that peripheral and central axotomy (no regenerative effect) triggered differential 5-hmC changes that are associated with distinct signaling pathways. 5-hmC was altered in half of regeneration-associated genes (RAGs), supporting its role for RAG regulation. Our analyses predicted transcription factors HIF-1, STAT and IRF that may collaborate with Tet3 for 5-hmC modifications. Intriguingly, central axotomy lead to widespread 5-hmC modifications with little overlap with peripheral axotomy, thus potentially constituting a roadblock for regeneration. Our study revealed 5-hmC as a previously unrecognized epigenetic mechanism underlying the divergent responses after axonal injury.

2016-12-09 | GSE85972 | GEO

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