ArticleBMC cancer2015
M1 and M2 macrophages derived from THP-1 cells differentially modulate the response of cancer cells to etoposide.
Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 623 papers, 2 of them syntheses that pooled it.
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Who cites it
623 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,094 citations in OpenAlex.
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- Engineering a PD-L1-sensing synthetic receptor for programmable macrophage response.Journal of biological engineering · 2026Article
- Induced chromosomal instability in triple negative breast cancer cells promotes M2-like polarization of macrophages.Scientific reports · 2026Article
- CSF1R inhibitors mitigate CDK4/6 inhibitor-induced immunosuppression to increase antitumor immunity in HR+/HER2- breast cancer.Oncogene · 2026Article
- Intestinal epithelial PIEZO1 regulates macrophage-to-myofibroblast transition via epithelial-derived TGF-α signaling in Crohn's disease.Cell communication and signaling : CCS · 2026Article
- Macrophage-derived fibronectin suppresses antitumor immunity via tissue stiffening and immunosuppressive cell induction in cancer mouse models.Nature communications · 2026Article
- Tumor-associated protease-activated anti-CD47 antibody precisely maintains phagocytic ability of macrophages with minimal effect on healthy tissue.Journal of translational medicine · 2026Article
- Unfolding Immune Dysregulation in COPD: Identification of a Three-Gene Signature and Functional Validation ofInternational journal of molecular sciences · 2026Article
- Renin-angiotensin imbalance promotes excessive fibrin deposition through M2 macrophage-derived tissue factor expression in eosinophilic chronic rhinosinusitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
563 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTumor associated macrophages (TAMs) are present in high density in solid tumors. TAMs share many characteristics with alternatively activated macrophages, also called M2. They have been shown to favor tumor development and a role in chemoresistance has also been suggested. Here, we investigated the effects of M2 in comparison to M1 macrophages on cancer cell sensitivity to etoposide.
methodsWe set up a model of macrophage polarization, starting from THP-1 monocytes differentiated into macrophages using PMA (Phorbol 12-myristate 13-acetate). Once differentiated (M0 macrophages), they were incubated with IL-4 and IL-13 in order to obtain M2 polarized macrophages or with IFN-gamma and LPS for classical macrophage activation (M1). To mimic the communication between cancer cells and TAMs, M0, M1 or M2 macrophages and HepG2 or A549 cancer cells were co-cultured during respectively 16 (HepG2) or 24 (A549) hours, before etoposide exposure for 24 (HepG2) or 16 (A549) hours. After the incubation, the impact of etoposide on macrophage polarization was studied and cancer cell apoptosis was assessed by western-blot for cleaved caspase-3 and cleaved PARP-1 protein, caspase activity assay and FACS analysis of Annexin V and PI staining.
resultsmRNA and protein expression of M1 and M2 markers confirmed the polarization of THP-1-derived macrophages, which provide a new, easy and well-characterized model of polarized human macrophages. Etoposide-induced cancer cell apoptosis was markedly reduced in the presence of THP-1 M2 macrophages, while apoptosis was increased in cells co-cultured with M1 macrophages. On the other hand, etoposide did not influence M1 or M2 polarization.
conclusionsThese results evidence for the first time a clear protective effect of M2 on the contrary to M1 macrophages on etoposide-induced cancer cell apoptosis.
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