Interleukin-17 Receptor D in Physiology, Inflammation and Cancer

Girondel, Charlotte; Meloche, Sylvain

doi:10.3389/fonc.2021.656004

Cited by 15 publications

(17 citation statements)

References 52 publications

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“…New evidence suggests that P2RX7 has an essential role in restraining tumor progression [63]. Moreover, in vitro studies have shown that IL17RD, another ARL11-related protein (score = 0.7), exerts inhibitory effects on MAPK signaling to restrain the proliferation of various cancer cell lines [64]. Genes associated with MAPK regulation, caspase activation, and tumorigenesis are also part of the ARL11 interactive network, highlighting its pivotal role in the regulation of immune and cancer-related pathways (Figure 7).…”

Section: Discussionmentioning

confidence: 99%

Unraveling the Relevance of ARL GTPases in Cutaneous Melanoma Prognosis through Integrated Bioinformatics Analysis

Brito¹,

Costa-Silva

Barral

et al. 2021

IJMS

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Cutaneous melanoma (CM) is the deadliest skin cancer, whose molecular pathways underlying its malignancy remain unclear. Therefore, new information to guide evidence-based clinical decisions is required. Adenosine diphosphate (ADP)-ribosylation factor-like (ARL) proteins are membrane trafficking regulators whose biological relevance in CM is undetermined. Here, we investigated ARL expression and its impact on CM prognosis and immune microenvironment through integrated bioinformatics analysis. Our study found that all 22 ARLs are differentially expressed in CM. Specifically, ARL1 and ARL11 are upregulated and ARL15 is downregulated regardless of mutational frequency or copy number variations. According to TCGA data, ARL1 and ARL15 represent independent prognostic factors in CM as well as ARL11 based on GEPIA and OncoLnc. To investigate the mechanisms by which ARL1 and ARL11 increase patient survival while ARL15 reduces it, we evaluated their correlation with the immune microenvironment. CD4+ T cells and neutrophil infiltrates are significantly increased by ARL1 expression. Furthermore, ARL11 expression was correlated with 17 out of 21 immune infiltrates, including CD8+ T cells and M2 macrophages, described as having anti-tumoral activity. Likewise, ARL11 is interconnected with ZAP70, ADAM17, and P2RX7, which are implicated in immune cell activation. Collectively, this study provides the first evidence that ARL1, ARL11, and ARL15 may influence CM progression, prognosis, and immune microenvironment remodeling.

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Section: Discussionmentioning

confidence: 99%

Unraveling the Relevance of ARL GTPases in Cutaneous Melanoma Prognosis through Integrated Bioinformatics Analysis

Brito¹,

Costa-Silva

Barral

et al. 2021

IJMS

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“…ERK, JNK, as well as p38 pathways are also activated by IL-17B [ 87 ]. IL-17RD has been shown to both regulate IL-17 pathway signaling, as well as negatively regulate NF-κB and IRF signaling pathways downstream of TLRs [ 31 , 88 , 89 ]. The domains of IL-17RD have been proposed to interact with ERK1/2 MAPK cascade to inhibit fibroblast growth factor signaling [ 89 , 90 ].…”

Section: Signaling Events Following Il-17 Cytokine–receptor Engagementmentioning

confidence: 99%

“…IL-17RD has been shown to both regulate IL-17 pathway signaling, as well as negatively regulate NF-κB and IRF signaling pathways downstream of TLRs [ 31 , 88 , 89 ]. The domains of IL-17RD have been proposed to interact with ERK1/2 MAPK cascade to inhibit fibroblast growth factor signaling [ 89 , 90 ]. When the IL-17RA and IL-17-RD complex is stimulated by IL-17A, IL-17RD sequesters ACT1, disrupting the ACT1/TRAF6 signaling complex, leading to differential regulation of NF-κB and p38 MAPK pathways [ 89 , 91 , 92 ].…”

Section: Signaling Events Following Il-17 Cytokine–receptor Engagementmentioning

confidence: 99%

“…The domains of IL-17RD have been proposed to interact with ERK1/2 MAPK cascade to inhibit fibroblast growth factor signaling [ 89 , 90 ]. When the IL-17RA and IL-17-RD complex is stimulated by IL-17A, IL-17RD sequesters ACT1, disrupting the ACT1/TRAF6 signaling complex, leading to differential regulation of NF-κB and p38 MAPK pathways [ 89 , 91 , 92 ]. IL-17A signaling through the IL-17RA and IL-17RD complex regulates proinflammatory gene expression in cell-type-dependent manner.…”

Section: Signaling Events Following Il-17 Cytokine–receptor Engagementmentioning

confidence: 99%

“…IL-17A signaling through the IL-17RA and IL-17RD complex regulates proinflammatory gene expression in cell-type-dependent manner. IL-17A signal transduction mediated by the IL-17RA and IL-17RD complex competes with IL-17A-induced signaling dependent on TRAF6 recruitment to ACT1, reducing the activation of NF-κB transcription factor and dampening upregulation of IL-6 [ 31 , 89 , 92 ].…”

Section: Signaling Events Following Il-17 Cytokine–receptor Engagementmentioning

confidence: 99%

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Interleukin-17 Family Cytokines in Metabolic Disorders and Cancer

Meehan

Wang

2022

Genes

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Interleukin-17 (IL-17) family cytokines are potent drivers of inflammatory responses. Although IL-17 was originally identified as a cytokine that induces protective effects against bacterial and fungal infections, IL-17 can also promote chronic inflammation in a number of autoimmune diseases. Research in the last decade has also elucidated critical roles of IL-17 during cancer development and treatment. Intriguingly, IL-17 seems to play a role in the risk of cancers that are associated with metabolic disorders. In this review, we summarize our current knowledge on the biochemical basis of IL-17 signaling, IL-17′s involvement in cancers and metabolic disorders, and postulate how IL-17 family cytokines may serve as a bridge between these two types of diseases.

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The role of IL-17 in the pathogenesis and treatment of glioblastoma—an update on the state of the art and future perspectives

Łaszczych,

Czernicka,

Gostomczyk

et al. 2024

Med Oncol

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Glioblastoma (GBM) is the most common malignant brain tumor, which, despite significant progress made in the last years in the field of neuro-oncology, remains an incurable disease. GBM has a poor prognosis with a median survival of 12–15 months, and its aggressive clinical course is related to rapid growth, extensive infiltration of adjacent tissues, resistance to chemotherapy, radiotherapy and immunotherapy, and frequent relapse. Currently, several molecular biomarkers are used in clinical practice to predict patient prognosis and response to treatment. However, due to the overall unsatisfactory efficacy of standard multimodal treatment and the remaining poor prognosis, there is an urgent need for new biomarkers and therapeutic strategies for GBM. Recent evidence suggests that GBM tumorigenesis is associated with crosstalk between cancer, immune and stromal cells mediated by various cytokines. One of the key factors involved in this process appears to be interleukin-17 (IL-17), a pro-inflammatory cytokine that is significantly upregulated in the serum and tissue of GBM patients. IL-17 plays a key role in tumorigenesis, angiogenesis, and recurrence of GBM by activating pro-oncogenic signaling pathways and promoting cell survival, proliferation, and invasion. IL-17 facilitates the immunomodulation of the tumor microenvironment by promoting immune cells infiltration and cytokine secretion. In this article we review the latest scientific reports to provide an update on the role of IL-17 role in tumorigenesis, tumor microenvironment, diagnosis, prognosis, and treatment of GBM.

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Interleukin-17 Receptor D in Physiology, Inflammation and Cancer

Cited by 15 publications

References 52 publications

Unraveling the Relevance of ARL GTPases in Cutaneous Melanoma Prognosis through Integrated Bioinformatics Analysis

Unraveling the Relevance of ARL GTPases in Cutaneous Melanoma Prognosis through Integrated Bioinformatics Analysis

Interleukin-17 Family Cytokines in Metabolic Disorders and Cancer

The role of IL-17 in the pathogenesis and treatment of glioblastoma—an update on the state of the art and future perspectives

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