Correction to: Aryl hydrocarbon receptor signaling promotes ORMDL3-dependent generation of sphingosine-1-phosphate by inhibiting sphingosine-1-phosphate lyase

Wang, Hsueh Chun; Wong, Tzu Hsuan; Wang, Li Ting; Su, Hsiang Han; Yu, Hsiu Yueh; Wu, Ai Hsuan; Lin, Yu; Chen, Hua Ling; Suen, Jau‐Ling; Hsu, Sung‐Chi; Chen, Li Chen; Zhou, Yufeng; Huang, Shau Ku

doi:10.1038/s41423-018-0040-0

Cited by 4 publications

(1 citation statement)

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“…381 Combining anti-PD-L1, anti-PD1, or anti-CTLA4 therapy with a DNMT inhibitor enhances the antitumor immune response of CD8 + T cells and promotes a type I interferon response; clinical trials combining methyltransferase inhibitors and ICIs have begun. 341,[382][383][384] Utilizing hypomethylating drugs to revitalize CD8 + T cells prior to immune checkpoint therapy could be a useful strategy.…”

Section: Epigenetic Modulation Of Tumor-infiltrating Lymphocytes (Tils)mentioning

confidence: 99%

Epigenetic regulation in the tumor microenvironment: molecular mechanisms and therapeutic targets

Yang

Wang

et al. 2023

Sig Transduct Target Ther

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Over decades, researchers have focused on the epigenetic control of DNA-templated processes. Histone modification, DNA methylation, chromatin remodeling, RNA modification, and noncoding RNAs modulate many biological processes that are crucial to the development of cancers. Dysregulation of the epigenome drives aberrant transcriptional programs. A growing body of evidence suggests that the mechanisms of epigenetic modification are dysregulated in human cancers and might be excellent targets for tumor treatment. Epigenetics has also been shown to influence tumor immunogenicity and immune cells involved in antitumor responses. Thus, the development and application of epigenetic therapy and cancer immunotherapy and their combinations may have important implications for cancer treatment. Here, we present an up-to-date and thorough description of how epigenetic modifications in tumor cells influence immune cell responses in the tumor microenvironment (TME) and how epigenetics influence immune cells internally to modify the TME. Additionally, we highlight the therapeutic potential of targeting epigenetic regulators for cancer immunotherapy. Harnessing the complex interplay between epigenetics and cancer immunology to develop therapeutics that combine thereof is challenging but could yield significant benefits. The purpose of this review is to assist researchers in understanding how epigenetics impact immune responses in the TME, so that better cancer immunotherapies can be developed.

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Section: Epigenetic Modulation Of Tumor-infiltrating Lymphocytes (Tils)mentioning

confidence: 99%

Epigenetic regulation in the tumor microenvironment: molecular mechanisms and therapeutic targets

Yang

Wang

et al. 2023

Sig Transduct Target Ther

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Metformin inhibits IgE‐ and aryl hydrocarbon receptor‐mediated mast cell activation in vitro and in vivo

Wang

Huang

2018

Eur J Immunol

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Metformin, an anti-diabetic drug, possesses anti-inflammatory property beyond its glucose-lowering activity, but its regulatory effect on mast cells and allergic responses remains unknown, wherein the aryl hydrocarbon receptor (AhR)-ligand axis is critical in controlling mast cell activation. Herein, we provide evidence supporting the role of metformin in modulating mast cell activation by FcεR1-, AhR-mediated signaling or their combination. Metformin at relatively low doses was shown to suppress FcεR1mediated degranulation, IL-13, TNF-α and sphingosine-1-phosphate (S1P) secretion in murine bone marrow-derived mast cells (BMMCs). In contrast, metformin at the same doses potently inhibited all parameters in mast cells stimulated with an AhR ligand, 5,11dihydroindolo[3,2-b]carbazole-6-carbaldehyde (FICZ). Further, metformin was shown to inhibit FcεR1-and AhR-mediated passive cutaneous anaphylaxis (PCA) in vivo, reversible by a S1P receptor 2 antagonist, JTE-013. Using AhR reporter cells, Huh7-DRE-Luc cells, a human mast cell line, HMC-1, and BMMCs, metformin's inhibitory effect was mediated through the suppression of FICZ-induced AhR activity, calcium mobilization and ROS generation. Notably, FICZ-mediated oxidation of S1P lyase (S1PL) and its reduced activity were reversed by metformin, resulting in decreased levels of S1P. Collectively, these results suggested the potential utility of metformin in treating allergic diseases, particularly in cases with comorbid type II diabetes mellitus.Keywords: Aryl hydrocarbon receptor r Mast cell r Metformin r Sphingosine-1-phosphate r Sphingosine-1-phosphate lyase Additional supporting information may be found online in the Supporting Information section at the end of the article. Abbreviations: AhR: aryl hydrocarbon receptor · FICZ: 5,11dihydroindolo[3,2-b]carbazole-6-carbaldehyde · Met: metformin · S1P: sphingosine-1-phosphate · S1PL: sphingosine-1-phosphate lyase

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PAHs increase the production of extracellular vesicles both in vitro in endothelial cells and in vivo in urines from rats

Goff

Lagadic‐Gossmann

Latour

et al. 2019

Environmental Pollution

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Correction to: Aryl hydrocarbon receptor signaling promotes ORMDL3-dependent generation of sphingosine-1-phosphate by inhibiting sphingosine-1-phosphate lyase

Cited by 4 publications

References 0 publications

Epigenetic regulation in the tumor microenvironment: molecular mechanisms and therapeutic targets

Epigenetic regulation in the tumor microenvironment: molecular mechanisms and therapeutic targets

Metformin inhibits IgE‐ and aryl hydrocarbon receptor‐mediated mast cell activation in vitro and in vivo

PAHs increase the production of extracellular vesicles both in vitro in endothelial cells and in vivo in urines from rats

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