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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE166347 | GEO | 2021/02/09

REPOSITORIES: GEO

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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

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

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 macrophage remodeling [miRNA-seq]

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

| PRJNA700582 | ENA

Human endometriotic lesion expression of the miR-144-3p/miR-451a cluster, its correlation with markers of cell survival and origin of lesion content.

Project description:Endometriosis is an inflammatory condition in which endometrial tissue grows in ectopic locations. Survival and growth of these ectopic lesions is associated with pain and infertility. MicroRNAs (miRNAs) have been postulated to play a role in the pathophysiology of the disease and we have previously demonstrated expression of miR-451 in human endometriotic lesion tissue. Here we report elevated expression of the miR-144-3p/miR-451a cluster in human endometriotic lesion tissue. Use of an endometriotic epithelial cell line (12Z) in which the miRNA processing enzyme, DROSHA, was knocked down resulted in an enrichment in the primary (pri) form of miR-144-3p but not that of pri-miR-451a. Using an experimental mouse model of endometriosis in which ectopic endometriotic lesions were deficient for both of these miRNAs revealed that miR-451a, but not miR-144-3p may be derived from exogenous sources such as the circulation/erythrocytes. Together, these data suggest that the miR-144-3p/miR-451a cluster is expressed in human endometriotic lesion tissue, the level of expression correlates with survival status of the lesion tissue and that miR-451a, but not miR-144-3p may be derived from exogenous sources such as erythrocytes.

| S-EPMC6584560 | biostudies-literature

Activated Stellate Cell Paracrine HGF Exacerbated Pancreatic Cancer Cell Ferroptosis Resistance.

Project description:As a refractory tumor, pancreatic carcinoma is more vulnerable to ferroptosis, a novel regulated cell death mode. However, the exact role of pancreatic stellate cells (PSCs) in pancreatic cancer ferroptosis is still unclear. Using the coculture system, we revealed that activated PSCs promote pancreatic cancer cell ferroptosis resistance. Mechanistically, activated PSCs secreted HGF, which further activated the HGF receptor, c-MET, in pancreatic cancer cells, prevented lipid peroxidation, and ultimately triggered pancreatic cancer cell ferroptosis resistance in vitro and in vivo. TCGA and GEPIA databases also revealed a strong correlation between c-MET and antiferroptosis indicators. Our study supplied the evidence for the cross-talk between activated PSCs and pancreatic cancer cells in ferroptosis, which suggested a strategy to inhibit PSC paracrine signaling for preventing pancreatic carcinoma ferroptosis resistance.

| S-EPMC9177329 | biostudies-literature

Dissecting the <i>miR-451a</i>-Mif Pathway in Endometriosis Pathophysiology Using a Syngeneic Mouse Model: Temporal Expression of Lesion Mif Receptors, Cd74 and Cxcr4.

Project description:Endometriosis is an enigmatic disease characterized by pain and infertility in which endometrial tissue grows in ectopic locations, predominantly the pelvic cavity. The pathogenesis and pathophysiology of endometriosis is complex and postulated to involve alterations in inflammatory, cell proliferation and post-transcriptional regulatory pathways among others. Our understanding on the pathogenesis and pathophysiology of endometriosis is further complicated by the fact that endometriosis can only be diagnosed by laparoscopy only after the disease has manifested. This makes it difficult to understand the true pathogenesis as a cause-and-effect relationship is difficult to ascertain. To aid in our understanding on endometriosis pathogenesis and pathophysiology, numerous rodent models have been developed. In this case, we discuss further assessment of a miR-451a-macrophage migration inhibitory factor (Mif) pathway which contributes to lesion survival. Specifically, we evaluate the temporal expression of lesion Mif receptors, Cd74 and Cxcr4 using host mice which express wild-type or miR-451a deficient lesions. Similar to that observed in humans and a non-human primate model of endometriosis, Cd74 expression is elevated in lesion tissue in a temporal fashion while that of Cxcr4 shows minimal increase during initial lesion establishment but is reduced later during the lifespan. Absence of miR-451a during initial lesion establishment is associated with an augmentation of Cd74, but no Cxcr4 expression. The data obtained in this study provide further support for a role of Mif receptors, Cd74 and Cxcr4 in the pathophysiology of endometriosis.

| S-EPMC9313350 | biostudies-literature

miR-144-5p and miR-451a Inhibit the Growth of Cholangiocarcinoma Cells Through Decreasing the Expression of ST8SIA4.

Project description:Accumulating evidences indicate that non-coding RNAs play crucial roles in the progression of an extensive range of carcinomas. This study aimed to investigate the action mechanism of miR-144-5p and miR-451a in cholangiocarcinoma. We found that miR-144-5p and miR-451a were significantly decreased in cholangiocarcinoma patient samples compared to the adjacent normal bile duct samples. The downregulation of these two miRNAs was correlated with a more advanced disease state of cholangiocarcinoma patients. Overexpression of miR-144-5p and miR-451a suppressed the proliferation, invasion and migration of cholangiocarcinoma cells in vitro and inhibited xenograft tumor growth. Knockdown of these two miRNAs had the opposite effects. miR-144-5p and miR-451a regulated the expression of ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 4 (ST8SIA4), and presented a correlation with ST8SIA4 in patient samples. Overexpression of ST8SIA4 promoted the proliferation, invasion and migration of cholangiocarcinoma cells, and the changes were reversed by upregulating the expression of miR-144-5p and miR-451a. Our findings indicated that miR-144-5p and miR-451a displayed a tumor suppressor role through decreasing the expression of ST8SIA4 in cholangiocarcinoma.

| S-EPMC7841262 | biostudies-literature

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