ArticleCell division2025
Maraviroc enhances Bortezomib sensitivity in multiple myeloma by inhibiting M2 macrophage polarization via PI3K/AKT/RhoA signaling pathway in macrophages.
Article in Cell division, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Targeting METTL3/m6A/SOCS3 axis reprograms tumor-associated macrophage polarization to potentiate the efficacy of anti-PD-1 therapy in multiple myeloma.Cellular and molecular life sciences : CMLS · 2026Article
- Drug Resistance in Multiple Myeloma: Tumor-Intrinsic Mechanisms and the Bone Marrow Microenvironment.Cell biochemistry and function · 2026Review
- Oncometabolites and Hypoxia-Regulated Exosomes Shape HIF-Driven Macrophage Programs Across Type 2 Diabetes, Atherosclerosis, and Cancer.International journal of molecular sciences · 2026Review
- Macrophage polarization in hematologic cancers: mechanisms and therapeutic strategies.Blood research · 2026Review
- Biomechanical signaling of cytoskeleton and membrane reorganization in tumor immune chemotactic migration.Theranostics · 2026Review
- Quantitative phosphoproteomic profiling of CCL5/CCR5 signaling cascade in melanoma cells.Frontiers in oncology · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundMultiple myeloma (MM) is a malignancy where drug resistance often leads to relapse or refractory disease. Chemokine receptor 5 (CCR5) has emerged as a novel therapeutic target. However, the role of CCR5-antagonist Maraviroc (MVC) in M2 macrophage polarization and its potential to enhance Bortezomib sensitivity in MM has not been fully explored.
methodsWe used human bone marrow samples, RPMI 8226 cells, and THP-1 monocytes to investigate CCL3/CCR5 axis. ELISA measured CCL3/CCR5 levels. Knockdown/overexpression vectors modulated expression. Cell proliferation, apoptosis, and macrophage polarization were assessed using CCK8, flow cytometry, and transwell assays. QRT-PCR analyzed CCL3 expression, and western blotting examined PI3K/AKT/RhoA signaling. CCR5 was targeted via siRNAs or MVC. NOD/SCID mouse model evaluated CCL3/CCR5 effects on macrophage polarization and MVC's impact on Bortezomib efficacy.
resultsCCL3, CCR5, and M2 macrophage markers are upregulated in MM patients, with CCL3/CCR5 expression correlating with M2 macrophage polarization. Myeloma-secreted CCL3 and paracrine CCR5 significantly promoted M2 macrophage polarization by activating PI3K/AKT/RhoA signaling, which in turn enhanced myeloma proliferation, inhibited apoptosis, and reduced Bortezomib sensitivity. MVC inhibited M2 macrophage polarization and improved Bortezomib sensitivity in vitro and xenograft mouse myeloma models.
conclusionsMVC reduced macrophage polarization and enhanced Bortezomib sensitivity in MM cells.
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