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Epigenetic silencing of miR-144/451a cluster contributes to HCC progression via paracrine HGF/MIF-mediated macrophage remodeling [miRNA-seq]

ABSTRACT: Epigenetic silencing of miR-144/451a cluster contributes to HCC progression via paracrine HGF/MIF-mediated macrophage remodeling [miRNA-seq]

PROVIDER: PRJNA700582 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13650247.fastq.gz	Fastqsanger.gz
	SRR13650248.fastq.gz	Fastqsanger.gz
	SRR13650249.fastq.gz	Fastqsanger.gz
	SRR13650250.fastq.gz	Fastqsanger.gz
	SRR13650251.fastq.gz	Fastqsanger.gz

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Epigenetic silencing of miR-144/451a cluster contributes to HCC progression via paracrine HGF/MIF-mediated macrophage remodeling

Project description:Epigenetic silencing of miR-144/451a cluster contributes to HCC progression via paracrine HGF/MIF-mediated macrophage remodeling

| PRJNA700576 | ENA

Epigenetic silencing of miR-144/451a cluster contributes to HCC progression via paracrine HGF/MIF-mediated macrophage remodeling [mRNA]

Project description:Epigenetic silencing of miR-144/451a cluster contributes to HCC progression via paracrine HGF/MIF-mediated macrophage remodeling [mRNA]

| PRJNA700581 | ENA

Epigenetic silencing of miR-144/451a cluster contributes to HCC progression via paracrine HGF/MIF-mediated TAM remodeling.

Project description:Background & aimsHepatocellular carcinoma (HCC) is among the malignancies with the highest mortality. The key regulators and their interactive network in HCC pathogenesis remain unclear. Along with genetic mutations, aberrant epigenetic paradigms, including deregulated microRNAs (miRNAs), exert profound impacts on hepatocyte transformation and tumor microenvironment remodeling; however, the underlying mechanisms are largely uncharacterized.MethodsWe performed RNA sequencing on HCC specimens and bioinformatic analyses to identify tumor-associated miRNAs. The miRNA functional targets and their effects on tumor-infiltrating immune cells were investigated. The upstream events, particularly the epigenetic mechanisms responsible for miRNA deregulation in HCC, were explored.ResultsThe miR-144/miR-451a cluster was downregulated in HCC and predicted a better HCC patient prognosis. These miRNAs promoted macrophage M1 polarization and antitumor activity by targeting hepatocyte growth factor (HGF) and macrophage migration inhibitory factor (MIF). The miR-144/miR-451a cluster and EZH2, the catalytic subunit of polycomb repressive complex (PRC2), formed a feedback circuit in which miR-144 targeted EZH2 and PRC2 epigenetically repressed the miRNA genes via histone H3K27 methylation of the promoter. The miRNA cluster was coordinately silenced by distal enhancer hypermethylation, disrupting chromatin loop formation and enhancer-promoter interactions. Clinical examinations indicated that methylation of this chromatin region is a potential HCC biomarker.ConclusionsOur study revealed novel mechanisms underlying miR-144/miR-451a cluster deregulation and the crosstalk between malignant cells and tumor-associated macrophages (TAMs) in HCC, providing new insights into HCC pathogenesis and diagnostic strategies.

| S-EPMC7927270 | biostudies-literature

Epigenetic silencing of miR-144/451a cluster contributes to HCC progression via paracrine HGF/MIF-mediated macrophage remodeling

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

2021-02-09 | GSE166349 | GEO

MicroRNA-451a Regulates Myogenesis by Suppressing SPARC Expression Levels

Project description:MicroRNAs (miRNAs) are small noncoding RNAs that critically regulate gene expression. Their abundance and function have been linked to processes such as senescence and aging. In aged monkey muscle, miR-451a and miR-144-3p were highly upregulated compared to young animals. This led us to hypothesize that the miRNAs 451a/144-3p may be involved in muscle differentiation. We found that these miRNAs are downregulated during the differentiation of C2C12 myoblasts. Overexpression of miR-451a, but not miR-144-3p, robustly impeded the differentiation, suggesting an inhibitory role for miR-451a. We further investigated the potential regulatory targets of miR-451a and identified Sparc mRNA, encoding a secreted protein acidic and rich in cysteine (SPARC), which is involved in wound healing and cellular differentiation. Interestingly, we found that miR-451a suppresses Sparc mRNA translation according to the analysis of polysome profile. Our findings show that miR-451a is downregulated in differentiated myoblasts and decreases C2C12 differentiation at least in part by the suppression of SPARC biosynthesis.

2019-04-03 | GSE119186 | GEO

Epigenetic silencing of miR-144/451a cluster contributes to HCC progression via paracrine HGF/MIF-mediated macrophage remodeling [mRNA]

Project description:TAMs of tumor-bearing mice were isolated via FACS, and RNA was extracted and sequencing was performed at Genergy Co., Ltd.

2021-02-09 | GSE166347 | GEO

Epigenetic silencing of miR-144/451a cluster contributes to HCC progression via paracrine HGF/MIF-mediated macrophage remodeling [miRNA-seq]

Project description:The HCC and adjacent NH tissues were isolated from 9 HCC patients and RNA was extracted from the paired samples.

2021-02-09 | GSE166348 | GEO

Expression data of ECa9706 over expressing miR-144/451 cluster

Project description:miR-144/451 cluster is highly conversed in different species, miRbase database shows miR-144/451 cluster is constituted by miR-144-3p, miR-144-5p, miR-451a. Low-expression of miR-144/451 was closely related with the risk for esophageal cancer We used microarrays to identify the differentially expressed genes in ECa9706 over expressing miR-144/451 cluster

2018-08-08 | GSE118249 | GEO

Transcription profiling of wounds from ovariectomized MIF null mice and controls to investigate the role of MIF during wound healing using BALB/C MIF null mice

Project description:The aim of this experiment was to investigate the role of MIF during wound healing using BALB/C MIF null mice and in the context of reduced estrogen-associated impaired healing using ovariectomized mice (a mouse model of age-associated delayed healing). Ageing is associated with delayed cutaneous wound healing resulting from reduced estrogen levels. Macrophage migration inhibitory factor (MIF - NCBI RefSeq: NM_010798) is thought to mediate the effects of estrogen on wound healing. Gene expression was compared between wounds from ovariectomized MIF null mice and controls.

2005-11-05 | E-MEXP-209 | biostudies-arrayexpress

A Global Genomic View of MIF Knockdown Cell

Project description:siRNA-mediated knockdown of MIF expression in HEK293 cells resulted in inhibition of cell proliferation and cell cycle progress. The microarray study of MIF KD cells reveald knockdown of MIF would lead to extensive changes in gene expression profiles which may elucidate the molecular mechanism of MIF siRNA-mediated inhibition of cell cycle and cell proliferation. Keywords: The whole-genome expression analysis in MIF knockdown cells and the control cells HEK293 cells were transfected MIF siRNA (50pmol/ml & 100pmol/ml) or control RNA using LipofectamineTM 2000 reagent and re-incubated for 24 hours.At the designed time point, totol RNA was isolated from the different treated cells.The normal cells were used as control.

2009-11-02 | E-GEOD-10241 | biostudies-arrayexpress

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