Laricitrin ameliorates lung cancer-mediated dendritic cell suppression by inhibiting signal transducer and activator of transcription 3

Chang, Wei‐An; Hung, Jen‐Yu; Jian, Shu‐Fang; Lin, Yi-Shiuan; Wu, Cheng‐Ying; Hsu, Ya‐Ling; Kuo, Po‐Lin

doi:10.18632/oncotarget.13240

Cited by 15 publications

(8 citation statements)

References 40 publications

(49 reference statements)

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“…Frustratingly, accumulated evidence has suggested that tumor cells could suppress the immunological function of infiltrated DCs through the secretion of chemokines and cytokines, as well as inflammatory factors. Chang et al reported that tumor-infiltrating DCs are always functionally deficient [23]. Consistently in this study, we found that TCM-pretreated DCs expressed a lower frequency of maturation markers, including CD80, CD83, CD86, CD40 and MHC-II, compared with NHA mediumpretreated DCs (Fig.…”

Section: Discussionsupporting

confidence: 91%

Suppressor of cytokine signaling 1 inhibits the maturation of dendritic cells involving the nuclear factor kappa B signaling pathway in the glioma microenvironment

Xing-sheng

Luo

et al. 2020

Clinical and Experimental Immunology

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Summary Recurrence and diffuse infiltration challenge traditional therapeutic strategies for malignant glioma. Immunotherapy appears to be a promising approach to obtain long‐term survival. Dendritic cells (DCs), the most specialized and potent antigen‐presenting cells (APCs), play an important part in initiating and amplifying both the innate and adaptive immune responses against cancer cells. However, cancer cells can escape from immune surveillance by inhibiting maturation of DCs. Until the present, molecular mechanisms of maturation inhibition of DCs in the tumor microenvironment (TME) have not been fully revealed. Our study showed that pretreatment with tumor‐conditioned medium (TCM) collected from supernatant of primary glioma cells significantly suppressed the maturation of DCs. TCM pretreatment significantly changed the morphology of DCs, TCM decreased the expression levels of CD80, CD83, CD86 and interleukin (IL)‐12p70, while it increased the expression levels of IL‐10, transforming growth factor (TGF)‐β and IL‐6. RNA‐Seq showed that TCM pretreatment significantly increased the gene expression level of suppressor of cytokine signaling 1 (SOCS1) in DCs. suppressor of cytokine signaling 1 (SOCS1) knock‐down significantly antagonized the maturation inhibition of DCs by TCM, which was demonstrated by the restoration of maturation markers. TCM pretreatment also significantly suppressed T cell viability and T helper type 1 (Th1) response, and SOCS1 knock‐down significantly antagonized this suppressive effect. Further, TCM pretreatment significantly suppressed p65 nuclear translocation and transcriptional activity in DCs, and SOCS1 knock‐down significantly attenuated this suppressive effect. In conclusion, our research demonstrates that TCM up‐regulate SOCS1 to suppress the maturation of DCs via the nuclear factor‐kappa signaling pathway.

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Section: Discussionsupporting

confidence: 91%

Suppressor of cytokine signaling 1 inhibits the maturation of dendritic cells involving the nuclear factor kappa B signaling pathway in the glioma microenvironment

Xing-sheng

Luo

et al. 2020

Clinical and Experimental Immunology

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“…The STATs pathway has been shown to play an essential role in the downregulation of inflammatory responses in AD ( Bao et al ., 2013 ; Chang et al ., 2016 ). Activation of STAT3 resulted in increased release of TNF-α, IL-10, IL-1β ( Zhang et al ., 2015 ; Drennan et al ., 2016).…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effect of Carnosol on Phthalic Anhydride-Induced Atopic Dermatitis via Inhibition of STAT3

Lee

Hwang

Choi

et al. 2017

Biomolecules & Therapeutics

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Carnosol is a phenolic antioxidant present in rosemary (Rosmarinus officinalis). It is known for anti-inflammatory effects, analgesic activity and anti-cancer effects. However, no study has been dedicated yet to its effect on atopic dermatitis (AD). Here, we show that carnosol effectively inhibited LPS-induced nitric oxide (NO) generation and expression of inflammatory marker proteins (iNOS and COX-2) in RAW 264.7 cells. In addition, carnosol effectively inhibits the phosphorylation of STAT3 and DNA binding activity in RAW 264.7 cells. Pull down assay and docking model analysis showed that carnosol directly binds to the DNA binding domain (DBD) of STAT3. We next examined the anti-atopic activity of carnosol (0.05 μg/cm2) using 5% Phthalic anhydride (PA)-induced AD model in HR1 mice. Carnosol treatment significantly reduced 5% PA-induced AD like skin inflammation in skin tissues compared with control mice. Moreover, carnosol treatment inhibits the expression of iNOS and COX-2 in skin tissue. In addition, the levels of TNF-α, IL-1β, and Immunoglobulin-E in blood serum was significantly decreased in carnosol treated mice compared with those of 5% PA treated group. Furthermore, the activation of STAT3 in skin tissue was decreased in carnosol treated mice compared with control mice. In conclusion, these findings suggest that carnosol exhibited a potential anti-AD activity by inhibiting pro-inflammatory mediators through suppression of STAT3 activation via direct binding to DBD of STAT3.

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“…The STAT pathway plays an important role in blocking the inflammatory responses in AD [42]. Activation of STAT3 is responsible for increased expression of COX-2 and iNOS [43].…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effects of Bee Venom on Phthalic Anhydride-Induced Atopic Dermatitis

Oh¹

2020

J Acupunct Res

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Background: Atopic dermatitis (AD) is a chronic inflammatory condition which can be studied using phthalic anhydride (PA) to induce AD. Anti-inflammatory properties of bee venom (BV) wereinvestigated to determine whether it may be a useful treatment for AD. Methods: AD was induced by applying to pical PA to 8-week-old HR-1 mice (N = 50), then treating with (0.1, 0.25, and 0.5 µg) or without topical BV. Body weight, ear thickness histology, enzymelinked immune sorbent assay (serum IgE concentrations), Western blot analysis [inducible nitric oxide synthase, cyclooxygenase-2, IκB-α, phospho-IκB-α, c-Jun N-terminal kinase (JNK), phospho-JNK, p38, phospho-p38, extra cellular signal-regulated kinase (ERK), and phospho-ERK], and the pull down assay for immunoblotting (p50), were used to measure inflammatory mediators. Results: PA + BV (0.1, 0.25, and 0.5 μg) significantly decreased ear thickness without altering body weight. IgE concentrations decreased in the PA + BV (0.5 µg)-treated groups compared with PAtreatment. Tumor necrosis factor-α, interleukin-1β, inducible nitric oxide synthase, cyclooxygenase-2, phospho-IκB-α, phospho-JNK, p38, phospho-p38, and phospho-ERK, all decreased following treatment with PA + BV compared with the PA-treatment alone. p50 was upregulated in the PA + BV-treated groups compared with the PA-treated group. Furthermore, the number of mast cells decreased in the PA + BV-treated groups compared with the PA-treated group. Epidermal thickness was significantly lower in the PA + BV-treated group compared with PA treatment alone. Conclusion: BV maybe a useful anti-inflammatory treatment for AD.

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Laricitrin ameliorates lung cancer-mediated dendritic cell suppression by inhibiting signal transducer and activator of transcription 3

Cited by 15 publications

References 40 publications

Suppressor of cytokine signaling 1 inhibits the maturation of dendritic cells involving the nuclear factor kappa B signaling pathway in the glioma microenvironment

Suppressor of cytokine signaling 1 inhibits the maturation of dendritic cells involving the nuclear factor kappa B signaling pathway in the glioma microenvironment

Inhibitory Effect of Carnosol on Phthalic Anhydride-Induced Atopic Dermatitis via Inhibition of STAT3

Anti-Inflammatory Effects of Bee Venom on Phthalic Anhydride-Induced Atopic Dermatitis

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