{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shamekh MM"],"funding":["Egyptian Cultural and Educational Bureau","Karolinska Institutet","IngaBritt och Arne Lundbergs Forskningsstiftelse (Ingabritt and Arne Lundberg Research Foundation)","IngaBritt och Arne Lundbergs Forskningsstiftelse"],"pagination":["114"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12847883"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(1)"],"pubmed_abstract":["Glucocorticoids (GCs) are known for their anti-inflammatory potential, which includes the macrophage polarization into an anti-inflammatory and tissue remodeling state. GCs are routinely co-administered to cancer patients to alleviate the side effects of chemotherapy. However, it is not well known if GCs can modulate tumor-associated macrophages (TAMs) to promote tumor progression. Here, we show that dexamethasone (DEX) induces dose-dependent differentiation of THP-1 monocyte-derived anti-tumorigenic (M1) macrophages into pro-tumorigenic (M2-like) macrophages, even in the presence of M1 cues, and that DEX can repolarize fully differentiated M1 macrophages into an M2-like state. These macrophages have a cytokine profile similar to the pro-tumorigenic (M2) macrophages and can stimulate the p"],"journal":["Cell death & disease"],"pubmed_title":["Dexamethasone drives macrophage repolarization linked to increased triple-negative breast cancer aggressiveness."],"pmcid":["PMC12847883"],"funding_grant_id":["LU2022-0025"],"pubmed_authors":["Nalvarte I","Shamekh MM","Lindqvist B"],"additional_accession":[]},"is_claimable":false,"name":"Dexamethasone drives macrophage repolarization linked to increased triple-negative breast cancer aggressiveness.","description":"Glucocorticoids (GCs) are known for their anti-inflammatory potential, which includes the macrophage polarization into an anti-inflammatory and tissue remodeling state. GCs are routinely co-administered to cancer patients to alleviate the side effects of chemotherapy. However, it is not well known if GCs can modulate tumor-associated macrophages (TAMs) to promote tumor progression. Here, we show that dexamethasone (DEX) induces dose-dependent differentiation of THP-1 monocyte-derived anti-tumorigenic (M1) macrophages into pro-tumorigenic (M2-like) macrophages, even in the presence of M1 cues, and that DEX can repolarize fully differentiated M1 macrophages into an M2-like state. These macrophages have a cytokine profile similar to the pro-tumorigenic (M2) macrophages and can stimulate the p","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-06-09T06:56:36.121Z","creation":"2026-06-09T03:11:50.996Z"},"accession":"S-EPMC12847883","cross_references":{"pubmed":["41413093"],"doi":["10.1038/s41419-025-08363-9"]}}