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Macrophage populations enriched in the TME, especially M1 and M2 states, correlate with clinical outcomes. This study evaluates how pro-inflammatory M1- and immunosuppressive M2-derived EVs affect melanoma cells, using cytokine profiling, RNA-seq/qPCR, invasion and spheroid assays, confocal imaging, and western blotting.",{"@graph":69,"@context":126},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/extracellular-vesicles-derived-from-proinflammatory-m1-macrophages-induce-an-inflammatory-and-invasive-phenotype-in-melanoma-cells/457688/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/extracellular-vesicles-derived-from-proinflammatory-m1-macrophages-induce-an-inflammatory-and-invasive-phenotype-in-melanoma-cells/457688.png","ImageObject",300,407,{"name":92,"@type":93},"Mafia Boss","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-03","2026-09-30",true,{"@type":102,"interactionType":103,"userInteractionCount":81},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118,122],{"name":109,"@type":110,"acceptedAnswer":111},"What was the goal of comparing M1 and M2 macrophage-derived EVs in melanoma?","Question",{"text":112,"@type":113},"To determine how pro-inflammatory (M1) versus immunosuppressive (M2) macrophage EVs influence melanoma cell behavior and EV-mediated interactions within the TME.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How were macrophage-derived EVs obtained and analyzed in the study?",{"text":117,"@type":113},"EVs were isolated from conditioned media of THP-1 cells polarized to M0, M1, and M2 using ultracentrifugation, followed by cytokine array analysis for M0 and M1 EVs.",{"name":119,"@type":110,"acceptedAnswer":120},"What key effect did M1 EVs have on melanoma cells?",{"text":121,"@type":113},"M1 EVs reprogrammed melanoma cells toward a pro-inflammatory state by increasing expression and secretion of CXCL8, IL-6, and IL-1β, which enhanced invasion.",{"name":123,"@type":110,"acceptedAnswer":124},"Which signaling pathway links M1 EVs to inflammation-associated gene changes?",{"text":125,"@type":113},"M1 EV treatment activated the NF-κB signaling pathway, and inhibition using an IKK16 inhibitor reduced inflammation-associated gene expression.","https://schema.org",{"og:url":83,"og:type":128,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":130,"canonical":83},"index,follow",{"doc_id":132,"site_id":62},457688,1790903507,{"code":4,"msg":5,"data":135},{"doc_id":132,"user_id":136,"nickname":92,"user_avatar":137,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":138,"file_id":139,"file_url":140,"file_type":141,"file_size":142,"view_count":81,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":143,"language":144,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":145,"faqs":146,"seo_title":147,"seo_description":67,"update_tm":148,"read_time":149},962090760730,"https://ap-avatar.wpscdn.com/davatar_9964176cb1d06d4a9deccf72a44ae3dc","Mäki-Mantila etal. Cell Communication and Signaling (2026) 24:10  \n[https://doi.org/10.1186/s12964-025-02571-8](https://doi.org/10.1186/s12964-025-02571-8)  \nCell Communication and Signaling  \nRESEARCH Open Access  \nExtracellular vesicles derived from proinflammatory M1 macrophages induce an inflammatory and invasive phenotype in melanoma cells  \nKaisa Mäki-Mantila 1*, Einari A. Niskanen 1, Kirsi Kainulainen 1, Laia Puig Pardas 1, Niina Aaltonen 1, Wafa Wahbi2, PiiaTakabe 1, Aino Rönkä3,4, Kirsi Rilla 1,5 and Sanna Pasonen-Seppänen 1  \nAbstract  \nBackground Melanoma progression and metastasis depend on intercellular communication within the tumor microenvironment (TME), where extracellular vesicles (EVs) have emerged as essential mediators through the transfer of molecular cargo. In melanoma, macrophages are enriched in theTME, and their abundance and infiltration into the tumor area are associated with poor prognosis. In this study, we examined the effects of pro-inflammatory M1 and immunosuppressive M2 macrophage-derived EVs on melanoma cells to gain insights into EV-mediated interactions between macrophages and tumor cells.  \nMethods Macrophage-derived EVs were isolated by ultracentrifugation from the conditioned media ofTHP-1 cells polarized to M0, M1 and M2 macrophages. The cytokine content of M0 and M1 EVs was analyzed using a cytokine array. MV3 and COLO800 melanoma cells were treated with EVs to investigate their impact on gene expression using RNA-seq and qPCR. The functional effects of EVs on melanoma cells were assessed with invasion and spheroid assays, confocal imaging and western blotting.  \nResults Our results demonstrate that M1 EVs reprogrammed MV3 melanoma cells into a pro-inflammatory state by upregulating the gene expression and secretion of the pro-inflammatory cytokines CXCL8, IL-6 and IL-1β. This M1 EV-induced inflammatory phenotype enhanced melanoma cell invasion, which was suppressed by CXCL8 silencing. Furthermore, M1 EV treatment activated the NF-ĸB signaling pathway, and its inhibition with IKK16 inhibitor led to the downregulation of inflammation-associated genes.  \nConclusions Our findings suggest that M1 EVs promote tumor-associated inflammation in melanoma cells through NF-ĸB signaling. This underscores the pivotal role of EV-mediated macrophage–tumor cell communication in cancer progression.  \nKeywords Macrophage, Extracellular vesicle, Melanoma, Pro-tumor inflammation, Cell–cell communication  \n*Correspondence:  \nKaisa Mäki-Mantila[kaisa.maki-mantila@uef.fi](kaisa.maki-mantila@uef.fi)  \nFull list of author information is available at the end of the article  \n© The Author(s) 2025. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creati](http://creati)[vecommons.org/l](vecommons.org/l)icenses/by-nc-nd/4.0/.  \nMäki-Mantila et al. Cell Communication and Signaling (2026) 24:10  \nIntroduction  \nTumor microenvironment (TME) and its components facilitate melanoma progression through complex and dynamic intercellular communication. Extracellular vesicles (EVs) have emerged as important cel","cbCaitj5PEvDtdPS","https://ap.wps.com/l/cbCaitj5PEvDtdPS","pdf",5754373,17,"English","# Abstract\n## Background\n## Methods\n## Results\n## Conclusions\n# Introduction","[{\"question\":\"What was the goal of comparing M1 and M2 macrophage-derived EVs in melanoma?\",\"answer\":\"To determine how pro-inflammatory (M1) versus immunosuppressive (M2) macrophage EVs influence melanoma cell behavior and EV-mediated interactions within the TME.\"},{\"question\":\"How were macrophage-derived EVs obtained and analyzed in the study?\",\"answer\":\"EVs were isolated from conditioned media of THP-1 cells polarized to M0, M1, and M2 using ultracentrifugation, followed by cytokine array analysis for M0 and M1 EVs.\"},{\"question\":\"What key effect did M1 EVs have on melanoma cells?\",\"answer\":\"M1 EVs reprogrammed melanoma cells toward a pro-inflammatory state by increasing expression and secretion of CXCL8, IL-6, and IL-1β, which enhanced invasion.\"},{\"question\":\"Which signaling pathway links M1 EVs to inflammation-associated gene changes?\",\"answer\":\"M1 EV treatment activated the NF-κB signaling pathway, and inhibition using an IKK16 inhibitor reduced inflammation-associated gene expression.\"}]","Extracellular vesicles derived from proinflammatory M1 macrophages induce an inflammatory and invasive phenotype in melanoma cells | PDF",1790750153,43]