Aryl hydrocarbon receptor in association with RelA modulates IL-6 expression in non-smoking lung cancer

Ph, Chen; Chang, Hui; Jt, Chang; Lin, Pei

doi:10.1038/onc.2011.438

Cited by 55 publications

(64 citation statements)

References 55 publications

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“…1A). In the absence of exogenous ligand, AhR is associated with RelA and positively modulates NF-kB activity, as well as upregulates IL-6 expression, in H1355 cells (Chen et al, 2012). Here we further demonstrated that silencing of RelA expression not only abolishes AhR-enhanced interleukin expression (Fig.…”

Section: Resultssupporting

confidence: 57%

“…Here, we further demonstrated that knockdown of RelA or IL-6 expression by siRNA interference reduces AhRfacilitated colony formation of lung AD cells, confirming the involvement of RelA/IL-6 in AhR-promoted tumor growth. Our previous report demonstrated that upregulation of AhR reduces IkBa level (Chen et al, 2012). Treatment with 17-AAG not only increased the accumulation of IkBa protein, but also reduced IL-6/Il-8 expression and AhR protein, suggesting that 17-AAG inhibits RelA-dependent AhR-promoted tumor growth.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, we demonstrated that AhR increases NF-kB activity by direct association with RelA and thus upregulates IL-6 expression in lung AD cells (Chen et al, 2012). IL-6 has been shown to play a role in tumor progression (Smith et al, .…”

Section: Discussionmentioning

confidence: 99%

“…The target site of IL-6 is GCCACTCACCTCTTCAGAA. Transient overexpression of AhR in H1355 cells was previously described (Chen et al, 2012).After replacement with fresh media, cells were incubated at 37°C for an additional 48 hours prior to testing of gene expression.…”

Section: Methodsmentioning

confidence: 99%

“…Blocking AhR activation is considered a preventive mechanism for carcinogenesis (Ciolino and Yeh, 2001). Regardless of ligand activation, AhR upregulates expression of cytochrome P4501B1, fibroblast growth factor-9, and interleukin-6 in lung AD cells, and AhR expression is correlated with protein expressions of these regulated genes in lung AD (Chang et al, 2007;Wang et al, 2009;Chen et al, 2012). Due to the abundance of AhR in lung AD and its role in promoting growth of lung AD cells (Chang et al, 2007), we proposed that AhR is involved in the development of lung AD, raising the possibility of AhR as a therapeutic target for lung AD.…”

Section: Introductionmentioning

confidence: 99%

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Aryl Hydrocarbon Receptor is a Target of 17-Allylamino-17-demethoxygeldanamycin and Enhances its Anticancer Activity in Lung Adenocarcinoma Cells

Chen

Chang

et al. 2012

Mol Pharmacol

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Section: Resultssupporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Aryl Hydrocarbon Receptor is a Target of 17-Allylamino-17-demethoxygeldanamycin and Enhances its Anticancer Activity in Lung Adenocarcinoma Cells

Chen

Chang

et al. 2012

Mol Pharmacol

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Aryl hydrocarbon receptor mediates both proinflammatory and anti‐inflammatory effects in lipopolysaccharide‐activated microglia

Lee¹,

Lin

Hsu³

et al. 2015

Glia

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The aryl hydrocarbon receptor (AhR) regulates peripheral immunity; but its role in microglia-mediated neuroinflammation in the brain remains unknown. Here, we demonstrate that AhR mediates both anti-inflammatory and proinflammatory effects in lipopolysaccharide (LPS)-activated microglia. Activation of AhR by its ligands, formylindolo[3,2-b]carbazole (FICZ) or 3-methylcholanthrene (3MC), attenuated LPS-induced microglial immune responses. AhR also showed proinflammatory effects, as evidenced by the findings that genetic silence of AhR ameliorated the LPS-induced microglial immune responses and LPS-activated microglia-mediated neurotoxicity. Similarly, LPS-induced expressions of tumor necrosis factor α (TNFα) and inducible nitric oxide synthase (iNOS) were reduced in the cerebral cortex of AhR-deficient mice. Intriguingly, LPS upregulated and activated AhR in the absence of AhR ligands via the MEK1/2 signaling pathway, which effects were associated with a transient inhibition of cytochrome P450 1A1 (CYP1A1). Although AhR ligands synergistically enhance LPS-induced AhR activation, leading to suppression of LPS-induced microglial immune responses, they cannot do so on their own in microglia. Chromatin immunoprecipitation results further revealed that LPS-FICZ co-treatment, but not LPS alone, not only resulted in co-recruitment of both AhR and NFκB onto the κB site of TNFα gene promoter but also reduced LPS-induced AhR binding to the DRE site of iNOS gene promoter. Together, we provide evidence showing that microglial AhR, which can be activated by LPS, exerts bi-directional effects on the regulation of LPS-induced neuroinflammation, depending on the availability of external AhR ligands. These findings confer further insights into the potential link between environmental factors and the inflammatory brain disorders.

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An Insight into the Roles of Dietary Tryptophan and Its Metabolites in Intestinal Inflammation and Inflammatory Bowel Disease

Zhang

Zabed

et al. 2021

Molecular Nutrition Food Res

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Inflammatory bowel disease (IBD) is complex, chronic, and relapsing gastrointestinal inflammatory disorders, which includes mainly two conditions, namely ulcerative colitis (UC) and Crohn's disease (CD). Development of IBD in any individual is closely related to his/her autoimmune regulation, gene‐microbiota interactions, and dietary factors. Dietary tryptophan (Trp) is an essential amino acid for intestinal mucosal cells, and it is associated with the intestinal inflammation, epithelial barrier, and energy homeostasis of the host. According to recent studies, Trp and its three major metabolic pathways, namely kynurenine (KYN) pathway, indole pathway, and 5‐hydroxytryptamine (5‐HT) pathway, have vital roles in the regulation of intestinal inflammation by acting directly or indirectly on the pro/anti‐inflammatory cytokines, functions of various immune cells, as well as the intestinal microbial composition and homeostasis. In this review, recent advances in Trp‐ and its metabolites‐associated intestinal inflammation are summarized. It further discusses the complex mechanisms and interrelationships of the three major metabolic pathways of Trp in regulating inflammation, which could elucidate the value of dietary Trp to be used as a nutrient for IBD patients.

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Aryl hydrocarbon receptor in association with RelA modulates IL-6 expression in non-smoking lung cancer

Cited by 55 publications

References 55 publications

Aryl Hydrocarbon Receptor is a Target of 17-Allylamino-17-demethoxygeldanamycin and Enhances its Anticancer Activity in Lung Adenocarcinoma Cells

Aryl Hydrocarbon Receptor is a Target of 17-Allylamino-17-demethoxygeldanamycin and Enhances its Anticancer Activity in Lung Adenocarcinoma Cells

Aryl hydrocarbon receptor mediates both proinflammatory and anti‐inflammatory effects in lipopolysaccharide‐activated microglia

An Insight into the Roles of Dietary Tryptophan and Its Metabolites in Intestinal Inflammation and Inflammatory Bowel Disease

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