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Loss of Histone Methyltransferase Ezh2 Exacerbates Polarization of Macrophages toward M2-Like Phenotypes by Hepatocellular Carcinoma [ATAC-seq]

ABSTRACT: The roles of epigenetic regulator Ezh2 in TAMs of liver cancer still unclear. In this study, our results demonstrated that the absence of Ezh2 in bone marrow-derived macrophages (BMDMs) exacerbated M2-like phenotypic changes upon incubation with conditioned media (CM) from hepatocellular carcinoma (HCC) cell line Hepa1-6. The ATAC-seq revealed that the promoter regions of pyruvate metabolic process-related genes were more accessible in treated BMDMs Ezh2 KO.

ORGANISM(S): Mus musculus

PROVIDER: GSE298839 | GEO | 2026/02/22

REPOSITORIES: GEO

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Loss of Histone Methyltransferase Ezh2 Exacerbates Polarization of Macrophages toward M2-Like Phenotypes by Hepatocellular Carcinoma [RNA-Seq]

Project description:The roles of histone methytransferase Ezh2 in TAMs of liver cancer still unclear. In this study, an RNA sequencing was performed for samples from bone marrow-derived macrophages (BMDMs) of WT and Ezh2 KO mice upon exposure to conditioned media (CM) from hepatocellular carcinoma (HCC) cell line Hepa1-6. The results demonstrated that the absence of Ezh2 in BMDMs exacerbated M2-like phenotypic changes upon incubation with CM from hepatocellular carcinoma (HCC) cell line. The RNA-sequencing revealed that the M2 gene set was further upregulated in treated BMDMs Ezh2 KO compared to treated BMDMs WT WT and the hallmark of Glycolysis as enriched pathway was identified in BMDMs Ezh2 KO. Additionally, the hallmark of IL-6/JAK/STAT pathway was enriched in CM-treated BMDMs. Collectively, these findings provide evidence that JAK/STAT3 axis is critical for M2-like phenotypic changes and Ezh2 suppresses the shifts of macrophage metabolism toward glycolysis that promotes M2 polarization.

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Loss of Histone Methyltransferase Ezh2 Exacerbates Polarization of Macrophages toward M2-Like Phenotypes by Hepatocellular Carcinoma [ATAC-seq]

Project description:Loss of Histone Methyltransferase Ezh2 Exacerbates Polarization of Macrophages toward M2-Like Phenotypes by Hepatocellular Carcinoma [ATAC-seq]

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Loss of Histone Methyltransferase Ezh2 Exacerbates Polarization of Macrophages toward M2-Like Phenotypes by Hepatocellular Carcinoma [RNA-Seq]

Project description:Loss of Histone Methyltransferase Ezh2 Exacerbates Polarization of Macrophages toward M2-Like Phenotypes by Hepatocellular Carcinoma [RNA-Seq]

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Mitochondrial DNA promotes M2 polarization of tumor associated macrophages and HCC resistance to sorafenib

Project description:Mitochondrial damage-associated molecular patterns (DAMPs) including mitochondrial DNA (mtDNA), TFAM (transcription factor A, mitochondrial), and ATP, play crucial roles in the regulation of inflammatory environment in human diseases. However, the role of mitochondrial DAMPs in the regulation of tumor microenvironment (TEM) remains unclear. Herein we demonstrate that infiltration of M2 type tumor-associated macrophages (TAMs) was correlated with the resistance of hepatocellular carcinoma (HCC) to sorafenib. We found that cell free mtDNA in the plasma was significantly increased in sorafenib-resistant HCC mice. Sorafenib induced mitochondrial dysfunction and promoted the release of mtDNA into extracellular matrix of HCC. The mtDNAs were retaken by macrophages in the TME of HCC, activated TLR9 signaling on the endosome, and hence promoted the activation of NF-κB and the polarization of TAMs into M2. Application of DNase I to digest mtDNAs or depletion of macrophages with clodronate liposomes reduced the infiltration of M2 macrophage, decreased the growth of HCC, and sensitized the tumors to sorafenib. Furthermore, we showed that blocking the activation of TLR9 enhanced the therapeutic effect of sorafenib in HCC. Together, in the current study, we demonstrate that sorafenib treatment leads to the release of mtDNAs into TME in HCC, which in turn facilitates the polarization of TAMs into M2 macrophages through TLR9 activation and aggravates the resistance of HCC to sorafenib. Our study reveals a novel mechanism underlying circulating mtDAMPs in remodeling HCC microenvironment by reprograming the TAMs and provides a new strategy for improving the therapeutic effect of sorafenib and overcoming its resistance in HCC.

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