ArticleMolecular biology reports2026
Lutein reverses M2 macrophages polarization and exhibits antitumor effects on human triple-negative breast cancer cells.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Tumour-Derived sEVs Promote Triple-Negative Breast Cancer Progression Associated with HAVCR2 Upregulation in Macrophages.Oncology research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundTriple-negative breast cancer (TNBC) remains a major therapeutic challenge due to the lack of established molecular targets and the presence of highly infiltrating tumor-associated macrophages (TAMs), particularly the immunosuppressive M2 phenotype that drives tumor progression. This study investigated the potential of lutein, a plant-derived carotenoid with anticancer properties, to repolarize human monocyte-derived M2 macrophages into the antitumor M1 phenotype and thereby modulate the TNBC tumor microenvironment. METHODS AND
resultsCD14 + monocytes isolated from peripheral blood mononuclear cells were differentiated into M1 or M2 macrophages using GM-CSF/IFN-γ/lipopolysaccharide or M-CSF/IL-4, respectively. Lutein's effects on macrophage polarization, cell proliferation, cell migration and cytokine secretion were evaluated using flow cytometry, MTT proliferation assays, migration assays and enzyme-linked immunosorbent assays (ELISAs) in MDA-MB-231 cells. Additionally, tumor-related protein expressions from MDA-MB-231 cells were analyzed using protein arrays. Lutein significantly reduced the proliferation and migration of MDA-MB-231 cells when co-cultured with M1/M2 macrophages compared to the untreated group. IL-4 stimulation increased the expression of M2 macrophage marker (CD206) and protumor cytokines (IL-10 and TGF-β1), but lutein effectively reduced these elevated molecules in IL-4-activated macrophages. Proteomic profiling revealed that lutein downregulated several protumor proteins (survivin, VEGF, BCL-X, M-CSF, MMP-9) and upregulated antitumor markers (FKHR and GM-CSF). Furthermore, lutein markedly reduced the secretion of proinflammatory and protumorigenic cytokines and chemokines (IL-6, IL-18BPa, CCL2, CCL8, CCL7, CCL3, CCL20, and CXCL8).
conclusionThese findings suggest that lutein reprograms M2 macrophages toward an M1-like phenotype and disrupts tumor-promoting signaling within the TNBC microenvironment, highlighting its potential as an adjunct therapeutic agent.
Indexed as
Identifiers
41543578What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.