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RNA m6A methylation orchestrates cancer growth and metastasis via macrophage reprogramming

ABSTRACT: The CD45+ immune-infiltrated cells in B16 tumors from WT or KO mice were enriched. Then, pooled samples of mice per group were analyzed by single cell RNA sequencing （scRNA-seq）

ORGANISM(S): Mus musculus

PROVIDER: GSE159156 | GEO | 2021/01/19

REPOSITORIES: GEO

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Proton irradiation orchestrates macrophage reprogramming through NF?B signaling.

Project description:Tumor-associated macrophages (TAMs) represent potential targets for anticancer treatments as these cells play critical roles in tumor progression and frequently antagonize the response to treatments. TAMs are usually associated to an M2-like phenotype, characterized by anti-inflammatory and protumoral properties. This phenotype contrasts with the M1-like macrophages, which exhibits proinflammatory, phagocytic, and antitumoral functions. As macrophages hold a high plasticity, strategies to orchestrate the reprogramming of M2-like TAMs towards a M1 antitumor phenotype offer potential therapeutic benefits. One of the most used anticancer treatments is the conventional X-ray radiotherapy (RT), but this therapy failed to reprogram TAMs towards an M1 phenotype. While protontherapy is more and more used in clinic to circumvent the side effects of conventional RT, the effects of proton irradiation on macrophages have not been investigated yet. Here we showed that M1 macrophages (THP-1 cell line) were more resistant to proton irradiation than unpolarized (M0) and M2 macrophages, which correlated with differential DNA damage detection. Moreover, proton irradiation-induced macrophage reprogramming from M2 to a mixed M1/M2 phenotype. This reprogramming required the nuclear translocation of NF?B p65 subunit as the inhibition of I?B? phosphorylation completely reverted the macrophage re-education. Altogether, the results suggest that proton irradiation promotes NF?B-mediated macrophage polarization towards M1 and opens new perspectives for macrophage targeting with charged particle therapy.

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RNA m5C methylation orchestrates BLCA progression via macrophage reprogramming.

Project description:Recently, epigenetics showed essential roles in tumour microenvironment (TME) and immunotherapy response, however, the functions of RNA 5-methylcytosine (m5C) modification in TME remains unknown. According to 13 m5C regulators, we evaluated 412 BLCA patients from The Cancer Genome Atlas (TCGA) database. The m5C score was constructed by unsupervised clustering analysis and principal component analysis (PCA) algorithms. Gene set variation analysis (GSVA), ESTIMATE algorithm, and immunohistochemical (IHC) staining were performed. Macrophage chemotaxis assay was used to assess the M2 macrophages. Among the 412 patients, the frequency of mutation was 13%. m5C regulators was expressed significantly in BLCA tissue compared with normal tissue. Then, two m5C methylation modification patterns were identified with dissimilar TME cell infiltration patterns. The C1 alteration pattern in the m5C cluster was connected with better survival. In addition, we found that NSUN6 was highly correlated with recruitment of macrophages via bioinformatics and IHC. Further experiment validated that NSUN6 promoted HDAC10 expression by mediating m5C methylation, inhibited the transcription of macrophage-associated chemokines and thus inhibited the recruitment of M2 macrophages. The m5C score constructed by m5C modification pattern showed that high m5C score group had a better prognosis. This study uncovered the significant roles of m5C modifications in modulating the TME and indicated that NSUN6 could inhibit the recruitment of M2 macrophages via m5C methylation, which provided novel insight into epigenetic regulation of TME and clinical suggestions for immunotherapeutic strategies.

| S-EPMC10424284 | biostudies-literature

RNA m6A methylation orchestrates cancer growth and metastasis via macrophage reprogramming

Project description:RNA m6A methylation orchestrates cancer growth and metastasis via macrophage reprogramming

| PRJNA667832 | ENA

Gene Expression in wild type and CCR5 knockout mice with lung metastasis

Project description:We have shown that C57BL/6J CCR5 knockout mice develop 30.4% ± 8.6% fewer B16 F10 lung nodules compared to wild type mice after the intravenous injection of 100,000 B16 F10 cells. We sought to understand this phenomenon by comparing gene expression in the lungs of these mice at 6, 24, and 48 hours after tumor injection. There were 6 groups or conditions (CCR5 - 6 hours, WT - 6 hours, CCR5 - 24 hours, WT - 24 hours, CCR5 - 48 hours, WT - 48 hour); each group had 4 to 5 mice. All of the mice were injected with 100,000 B16 F10 melanoma cells by tail vein. At the designated time, the mice were anesthetized with Avertin and their lungs were perfused with PBS. After this, the lungs were harvested and snap frozen in liquid nitrogen. They were kept at minus 80 degrees C until processing. mRNA was extracted as described below and equivalent amounts of mRNA (by weight) was pooled by group.

2013-10-25 | E-GEOD-51422 | biostudies-arrayexpress

c-Rel orchestrates energy-dependent epithelial and macrophage reprogramming in fibrosis.

Project description:Fibrosis is a common pathological feature of chronic disease. Deletion of the NF-κB subunit c-Rel limits fibrosis in multiple organs, although the mechanistic nature of this protection is unresolved. Using cell-specific gene-targeting manipulations in mice undergoing liver damage, we elucidate a critical role for c-Rel in controlling metabolic changes required for inflammatory and fibrogenic activities of hepatocytes and macrophages and identify Pfkfb3 as the key downstream metabolic mediator of this response. Independent deletions of Rel in hepatocytes or macrophages suppressed liver fibrosis induced by carbon tetrachloride, while combined deletion had an additive anti-fibrogenic effect. In transforming growth factor-β1-induced hepatocytes, c-Rel regulates expression of a pro-fibrogenic secretome comprising inflammatory molecules and connective tissue growth factor, the latter promoting collagen secretion from HMs. Macrophages lacking c-Rel fail to polarize to M1 or M2 states, explaining reduced fibrosis in RelΔLysM mice. Pharmacological inhibition of c-Rel attenuated multi-organ fibrosis in both murine and human fibrosis. In conclusion, activation of c-Rel/Pfkfb3 in damaged tissue instigates a paracrine signalling network among epithelial, myeloid and mesenchymal cells to stimulate fibrogenesis. Targeting the c-Rel-Pfkfb3 axis has potential for therapeutic applications in fibrotic disease.

| S-EPMC7116435 | biostudies-literature

Characterizing Macrophage Diversity in Metastasis-Bearing Lungs Reveals a Lipid-Associated Macrophage Subset

Project description:Single cell RNA sequencing was performed on CD45+Ly6G-CD64+MerTK+ macrophages isolated from the lungs of mice 5 weeks after transplantation of 4T1-Luc mammary gland tumors. The purpose of this study was to determine the unique macrophage subsets present in the lungs of mice bearing mammary tumor metastases.

2021-08-31 | GSE164302 | GEO

Expression data from WT and Trim24-deficient tumor-associated macrophage(TAM) sorted from B16 bearing mouse

Project description:We conducted gene expression profile analysis by using CD45+ CD11b+ F4/80+ TAM sorted from WT or Trim24-deficient B16 bearing mouse.Scatter diagram revealed the most prominent different expression of genes altered in TAM were associated with M2 genes.

2019-09-06 | GSE116566 | GEO

Increased expression of p53 with APR-246 (eprenetapopt) reprograms tumor-associated macrophages to promote the efficacy of immune checkpoint blockade

Project description:Expression of genes in sorted CD4, CD8 and non-T CD45 cells isolated from TME of B16 tumors in wildtype B6, APR-246 treated wildtype B6 and Super p53 mice.

2022-02-11 | GSE166637 | GEO

Single cell transcriptomics of the tumor immune microenvironment from checkpoint blockade-treated B16 tumors edited with control or TBK1-targeting sgRNAs.

Project description:To examine the effect of tumor-specific TBK1 loss on the tumor immune microenvironment, we performed scRNA-seq on CD45+ cells from B16 tumors from mice treated with anti-PD-1 compared to mice treated with isotype control (IgG).

2022-11-07 | GSE217274 | GEO

Schistosoma-pulmonary hypertension sorted macrophage gene expression

Project description:Alveolar and tissue macrophages were sorted from Schistosoma-exposed and unexposed mice. The mice were C57Bl6/J background. Schistosoma mansoni exposure was intraperitoneal sensitization and intravenous challenge with purified eggs (see Kumar et al. Am J Respir Crit Care Med. 2015;192(8):998-1008. doi: 10.1164/rccm.201410-1820OC. PMID: 26192556). Samples were pooled from N=5 animals per group. Cell sorting was performed on day 3 after IV challenge. Alveolar macrophages were identified as CD45+F4/80+CD11c+SiglecF+. Tissue macrophages were identified as CD45+F4/80+CD11b+SSClow. The RNA library was prepared using a Kappa Stranded mRNA-Seq kit. RNA sequencing was performed on an Ion Proton platform. Expression analysis was performed using Tophat-Bowtie-Cufflinks with Galaxy online.

2016-07-21 | E-GEOD-84651 | biostudies-arrayexpress

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