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http://purl.uniprot.org/citations/35939336http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/35939336http://www.w3.org/2000/01/rdf-schema#comment"Cancer immunoediting is defined as the integration of the immune system's dual host-protective and tumor-promoting roles, including three phases: elimination, equilibrium, and escape. Immune selective pressure causes tumor cells to lose major histocompatibility complex expression or acquire immunosuppressive gene expression, which promotes tumor immune evasion and tumor progression. Interleukin-17D (IL-17D), a member of the IL-17 family of cytokines, plays an important role in the host defense against infection and inflammation. However, the role of IL-17D in the progression of lung cancer remains unclear. In this study, we found that IL-17D was highly expressed in human lung cancer, and increased IL-17D expression was associated with tumor stage and short overall survival. IL-17D overexpression significantly promoted tumor growth in subcutaneous xenograft mouse models but only slightly affected cell proliferation in vitro. Using flow cytometry, we found that IL-17D overexpression enhances the recruitment of tumor-associated macrophages to the tumor microenvironment. Based on the expression profile of IL17D-overexpressing A549 cells, we found that IL-17D increased the expression levels of macrophage polarization- and recruitment-related genes through the MAPK signaling pathway. Moreover, inhibition of the p38 pathway blocked macrophage infiltration induced by IL-17D. These results suggest that IL-17D regulates the tumor immune microenvironment via the p38 MAPK signaling pathway, highlighting IL-17D as a potential therapeutic target for lung cancer."xsd:string
http://purl.uniprot.org/citations/35939336http://purl.org/dc/terms/identifier"doi:10.18632/aging.204208"xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/author"Huang Q."xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/author"Liu Z."xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/author"Liu J."xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/author"Lin Z."xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/author"Wei Y."xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/author"Zhang X."xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/author"Zhang W."xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/author"Wang H."xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/author"Zhu Z."xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/author"Du W."xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/date"2022"xsd:gYear
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/name"Aging (Albany NY)"xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/pages"6149-6168"xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/title"Interleukin-17D promotes lung cancer progression by inducing tumor-associated macrophage infiltration via the p38 MAPK signaling pathway."xsd:string
http://purl.uniprot.org/citations/35939336http://purl.uniprot.org/core/volume"14"xsd:string
http://purl.uniprot.org/citations/35939336http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/35939336
http://purl.uniprot.org/citations/35939336http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/35939336
http://purl.uniprot.org/uniprot/#_Q8TAD2-mappedCitation-35939336http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35939336
http://purl.uniprot.org/uniprot/Q8TAD2http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/35939336