{"entity": "researcher", "timestamp": "2026-09-26T23:35:06.773Z", "family": "Larsson", "given": "Rolf", "initials": "R", "orcid": "0000-0002-3427-4128", "affiliations": ["a Department of Medical Sciences, Division of Cancer Pharmacology and Computational Medicine , Uppsala University , Uppsala , Sweden."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/9fff77fefd914d1eb30f4e9e213ef094.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/9fff77fefd914d1eb30f4e9e213ef094"}}, "publications": [{"entity": "publication", "iuid": "cc860d6d4fb74e2abb79c804ececb5e3", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/cc860d6d4fb74e2abb79c804ececb5e3.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/cc860d6d4fb74e2abb79c804ececb5e3"}}, "title": "The anticancer effect of mebendazole may be due to M1 monocyte/macrophage activation via ERK1/2 and TLR8-dependent inflammasome activation.", "authors": [{"family": "Blom", "given": "Kristin", "initials": "K"}, {"family": "Senkowski", "given": "Wojciech", "initials": "W"}, {"family": "Jarvius", "given": "Malin", "initials": "M"}, {"family": "Berglund", "given": "Malin", "initials": "M"}, {"family": "Rubin", "given": "Jenny", "initials": "J"}, {"family": "Lenhammar", "given": "Lena", "initials": "L"}, {"family": "Parrow", "given": "Vendela", "initials": "V"}, {"family": "Andersson", "given": "Claes", "initials": "C"}, {"family": "Loskog", "given": "Angelica", "initials": "A"}, {"family": "Frykn\u00e4s", "given": "M\u00e5rten", "initials": "M"}, {"family": "Nygren", "given": "Peter", "initials": "P"}, {"family": "Larsson", "given": "Rolf", "initials": "R", "orcid": "0000-0002-3427-4128", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9fff77fefd914d1eb30f4e9e213ef094.json"}}], "type": "journal article", "published": "2017-08-00", "journal": {"title": "Immunopharmacol Immunotoxicol", "issn": "1532-2513", "volume": "39", "issue": "4", "pages": "199-210", "issn-l": "0892-3973"}, "abstract": "Mebendazole (MBZ), a drug commonly used for helminitic infections, has recently gained substantial attention as a repositioning candidate for cancer treatment. However, the mechanism of action behind its anticancer activity remains unclear. To address this problem, we took advantage of the curated MBZ-induced gene expression signatures in the LINCS Connectivity Map (CMap) database. The analysis revealed strong negative correlation with MEK/ERK1/2 inhibitors. Moreover, several of the most upregulated genes in response to MBZ exposure were related to monocyte/macrophage activation. The MBZ-induced gene expression signature in the promyeloblastic HL-60 cell line was strongly enriched in genes involved in monocyte/macrophage pro-inflammatory (M1) activation. This was subsequently validated using MBZ-treated THP-1 monocytoid cells that demonstrated gene expression, surface markers and cytokine release characteristic of the M1 phenotype. At high concentrations MBZ substantially induced the release of IL-1\u03b2 and this was further potentiated by lipopolysaccharide (LPS). At low MBZ concentrations, cotreatment with LPS was required for MBZ-stimulated IL-1\u03b2 secretion to occur. Furthermore, we show that the activation of protein kinase C, ERK1/2 and NF-kappaB were required for MBZ-induced IL-1\u03b2 release. MBZ-induced IL-1\u03b2 release was found to be dependent on NLRP3 inflammasome activation and to involve TLR8 stimulation. Finally, MBZ induced tumor-suppressive effects in a coculture model with differentiated THP-1 macrophages and HT29 colon cancer cells. In summary, we report that MBZ induced a pro-inflammatory (M1) phenotype of monocytoid cells, which may, at least partly, explain MBZ's anticancer activity observed in animal tumor models and in the clinic.", "doi": "10.1080/08923973.2017.1320671", "pmid": "28472897", "labels": [], "xrefs": [], "notes": [], "created": "2018-12-05T12:30:06.150Z", "modified": "2026-09-23T11:41:14.433Z"}]}