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

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

PROVIDER: PRJNA491734 | ENA |

REPOSITORIES: ENA

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MenSCs inhibit HCC growth through oncogenic pathway suppression via regulating 5-hmC in enhancer elements [hMeDIP-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 | GSE120141 | 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 [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 [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 [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

Integrated detection of both 5-mC and 5-hmC by high-throughput tag sequencing technology highlights methylation reprogramming of bivalent genes during cellular differentiation [MeDIP_hMeDIP]

Project description:5-methylcytosine (5-mC) can be oxidized to 5-hydroxymethylcytosine (5-hmC). Genome-wide profiling of 5-hmC thus far indicated 5-hmC may not only be an intermediate form of DNA demethylation but could also constitute an epigenetic mark per se. We describe a cost-effective and selective method to detect both the hydroxymethylation and methylation status of cytosines in more than 1.8 million MspI sites in the human genome. This method involves the selective glucosylation of 5-hmC residues, short-sequence tag generation and high-throughput sequencing. We tested this method by screening H9 human embryonic stem cells and their differentiated embroid body cells, and found that differential hydroxymethylation preferentially occur in bivalent genes during cellular differentiation. Especially, our results support hydroxymethylation can regulate key transcription regulators with bivalent marks through demethylation and affect cellular decision on choosing active or inactive state of these genes upon cellular differentiation. We developed a cost-effective and selective method to detect both the hydroxymethylation and methylation status of cytosines in more than 1.8 million MspI sites in the human genome. In order to validate the results generated by this method, we applied MeDIP-seq and hMeDIP-seq to screen H9 human embryonic stem cells in comparison with the newly developed method.

2012-12-20 | E-GEOD-41070 | biostudies-arrayexpress

Rapid reprogramming of epigenetic and transcriptional profiles in mammalian culture systems

Project description:5-hmC profiling of mouse embryonic fibroblasts before and during adaptation to cell culture conditions using hMeDIP-chip

2014-12-17 | E-MTAB-3177 | biostudies-arrayexpress

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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