Hmgb1-IL-23-IL-17-IL-6-Stat3 Axis Promotes Tumor Growth in Murine Models of Melanoma

Tang, Qiong; Li, Jian; Zhu, Hongfei; Li, Pan; Zou, Zhenwei; Xiao, Yin

doi:10.1155/2013/713859

Cited by 54 publications

(41 citation statements)

References 44 publications

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“…IL-23 is an important cytokine in Th17 cell regulation. In contrast to our data, IL-23 has been shown to promote tumor progression and prevent anti-tumor immunity [ 31 ]. IL-23 produced by macrophages promotes tumor growth by activating STAT-3 in the macrophages and Treg cells [ 32 ].…”

Section: Discussioncontrasting

confidence: 99%

IL-17 promoted the inhibition of medulloblastoma in mice by splenocyte injection

et al. 2015

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BackgroundInterleukin 17 (IL-17) is a proinflammatory cytokine produced by a new subset of activated CD4+ T cells, Th17 cells. We previously showed that increased Th17 cell populations were presented in human medulloblastoma-infiltrating T cells and peripheral blood. In this study, we attempted to address the possible role of Th17 cells in the biologic activity of IL-17 for tumor control.MethodsWe grafted fresh surgically obtained medulloblastoma into syngeneic athymic nude/nude mice. We intrapertonially injected splenocyte and murine IL-17 in mice on the second day. The tumor volume and the life spans of the mice were measured. Meanwhile, the IL-17, IL-6, IL-23, Ccl2, Ccl20 and IFN-gamma expression in the tumors was also examined by real-time PCR, Western blot and enzyme-linked immunosorbent assay.ResultsWe found that medulloblastoma growth in IL-17-injected mice was significantly inhibited compared to the non-IL-17 treated mice. In contrast to the IL-17 antitumor activity observed in mice injected with splenocytes, we observed that IFN-gamma, IL-6, IL-23, Ccl2, and Ccl20 proteins were significantly increased in tumor tissues of mice injected with IL-17.ConclusionsThese experiments suggest that IL-17 may promote splenocyte antitumor activity in medulloblastoma. We postulate that IL-17’s antitumor activity may be related to the increased protein levels of IFN-gamma, IL-6, IL-23, Ccl2, and Ccl20.

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Section: Discussioncontrasting

confidence: 99%

IL-17 promoted the inhibition of medulloblastoma in mice by splenocyte injection

et al. 2015

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“…This finding was consistent with the results of a previous study (50); in this previous study, it was revealed that the expression of ICAM-1 is reduced by anti-IL-17. Similarly, another study suggested that HMGB1 can stimulate the expression of IL-17 (51). These results indicated that the HMGB1-IL-17-ICAM1 pathway has a critical role in the inflammatory response of PM.…”

Section: Discussionmentioning

confidence: 75%

MicroRNA-381 reduces inflammation and infiltration of macrophages in polymyositis via downregulating HMGB1

et al. 2018

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The downregulation of microRNA (miR)-381 has been detected in various diseases. The present study aimed to investigate the effects, and underlying mechanisms of miR-381 on inflammation and macrophage infiltration in polymyositis (PM). A mouse model of experimental autoimmune myositis (EAM) was generated in this study. Hematoxylin and eosin staining was conducted to detect the inflammation of muscle tissues. In addition, ELISA and immunohistochemistry were performed to determine the expression levels of associated factors, and reverse transcription-quantitative polymerase chain reaction and western blotting were used to detect the expression levels of related mRNAs and proteins. A luciferase activity assay was used to confirm the binding of miR-381 and high mobility group box 1 (HMGB1) 3' untranslated region. Transwell assays were also performed to assess the migratory ability of macrophages. The results demonstrated that serum creatine kinase (s-CK), HMGB1 and cluster of differentiation (CD)163 expression in patients with PM were increased compared within healthy controls. Conversely, the expression levels of miR-381 were downregulated in patients with PM. Furthermore, high HMGB1 expression was associated with poor survival rate in patients with PM. In the mouse studies, muscle inflammation and CD163 expression were decreased in the anti-IL-17 and anti-HMGB1 groups, compared with in the EAM model group. The expression levels of s-CK, HMGB1, IL-17 and intercellular adhesion molecule (ICAM)-1 were also downregulated in response to anti-IL-17 and anti-HMGB1. These findings indicated that HMGB1 was closely associated with inflammatory responses. In addition, the present study indicated that transfection of macrophages with miR-381 mimics reduced the migration of inflammatory macrophages, and the expression levels of HMGB1, IL-17 and ICAM-1. Conversely, miR-381 inhibition exerted the opposite effects. The effects of miR-381 inhibitors were reversed by HMGB1 small interfering RNA. In conclusion, miR-381 may reduce inflammation and the infiltration of macrophages; these effects were closely associated with the downregulation of HMGB1.

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“…Melanoma, also termed malignant melanoma, is a common skin neoplasm caused by hyperplasia of abnormal melanocytes (13). Although China is one of the countries with a low incidence of melanoma, the growth rate of malignant melanoma has continued to increase over previous years (14).…”

Section: Discussionmentioning

confidence: 99%

Propofol promotes apoptosis and suppresses the HOTAIR-mediated mTOR/p70S6K signaling pathway in melanoma cells

et al. 2017

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Abstract.Propofol is an intravenous anesthetic, which is widely used in clinical anesthesia induction and maintenance and is critical in the sedation of patients. However, the functions and mechanisms of propofol on apoptosis of melanoma cells remain unclear. The present study investigated whether propofol promotes cell apoptosis and suppresses the HOX transcript antisense RNA (HOTAIR)-mediated mechanistic target of rapamycin (mTOR) pathway in melanoma cells. B16F10 cells were cultured with different concentrations (0-10 µM) of propofol for 24 or 48 h. Proliferation and apoptosis of B16F10 cells were detected using MTT assay and flow cytometry. The pcDNA 3

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Hmgb1-IL-23-IL-17-IL-6-Stat3 Axis Promotes Tumor Growth in Murine Models of Melanoma

Cited by 54 publications

References 44 publications

IL-17 promoted the inhibition of medulloblastoma in mice by splenocyte injection

IL-17 promoted the inhibition of medulloblastoma in mice by splenocyte injection

MicroRNA-381 reduces inflammation and infiltration of macrophages in polymyositis via downregulating HMGB1

Propofol promotes apoptosis and suppresses the HOTAIR-mediated mTOR/p70S6K signaling pathway in melanoma cells

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