ArticleBMC cancer2013
Exosome derived from epigallocatechin gallate treated breast cancer cells suppresses tumor growth by inhibiting tumor-associated macrophage infiltration and M2 polarization.
Article in BMC cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers.
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Who cites it
164 citing papers in PubMed, 265 citations in OpenAlex.
- Induced chromosomal instability in triple negative breast cancer cells promotes M2-like polarization of macrophages.Scientific reports · 2026Article
- Recent Progress in Exosome-Derived Nanocarriers for Breast Cancer Therapy: Advances, Translational Barriers, and Scale-Up Considerations.Pharmaceutical research · 2026Review
- Natural Products Targeting Key Molecular Hallmarks in Gastric Cancer: Focus on Apoptosis, Inflammation, and Chemoresistance.International journal of molecular sciences · 2026Review
- Exosomal crosstalk between breast cancer cells and tumor-associated macrophages: mechanisms and therapeutic implications.Molecular biology reports · 2026Review
- Harnessing nanomedicine to target NF-κB signalling in cancer: at the intersection of inflammatory signalling, metabolic reprogramming, and therapeutic innovation.Cell communication and signaling : CCS · 2026Review
- Enhancement of host anti-mycobacterial immunity by green tea hot-water extract is mediated through miR-9-5p-enriched lung extracellular vesicles.Frontiers in immunology · 2026Article
- Flavonoids and miRNA Modulation: A Novel Approach to Managing Cancer, Diabetes, Depression, and Neurological Disorders.BioMed research international · 2026Review
- A multidimensional landscape of extracellular vesicle-mediated tumor drug resistance: mechanisms, biomarkers, engineered drug delivery, and clinical translation.Extracellular vesicles and circulating nucleic acids · 2026Review
- Exosomal regulation of cellular reprogramming and polarization in the tumor microenvironment.Cancer cell international · 2025Review
- The Potential of Vitamin D and Epigallocatechin Gallate (EGCG) for the Treatment of Uterine Fibroids: Evidence From In Vitro to Clinical Studies.Molecular nutrition & food research · 2025Review
- Circular RNA Cdr1as Modulates Macrophage-Mediated Cardiac Reparative Function.Circulation research · 2025Article
- Review
- Targeting the Tumor Immune Microenvironment in Triple-Negative Breast Cancer: The Promise of Polyphenols.Cancers · 2025Review
- ERα-dependent crosstalk between macrophages and cancer cells potentiates vasculogenic mimicry and M2 macrophage polarization in bladder cancer.Cell communication and signaling : CCS · 2025Article
- Identification of potential human targets for epigallocatechin gallate through a novel protein binding site screening approach.Journal of molecular modeling · 2025Article
- Integration of active ingredients from traditional Chinese medicine with nano-delivery systems for tumor immunotherapy.Journal of nanobiotechnology · 2025Review
- SMARCC1 promotes M2 macrophage polarization and reduces ferroptosis in lung cancer by activating FLOT1 transcription.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Potential biological roles of exosomal non-coding RNAs in breast cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- A systematic review and meta-analysis of the effects of green tea extracts and polyphenols in female hormone-dependent cancers for benefit-risk evaluation.Frontiers in oncology · 2025Article
- The role of natural compounds in modulation of small extracellular vesicle biogenesis and lipid metabolism in cancer.Frontiers in molecular biosciences · 2025Review
104 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTumor-associated macrophages (TAM) play an important role in tumor microenvironment. Particularly, M2 macrophages contribute to tumor progression, depending on the expression of NF-κB. Tumor-derived exosomes can modulate tumor microenvironment by transferring miRNAs to immune cells. Epigallocatechin gallate (EGCG) has well known anti-tumor effects; however, no data are available on the influence of EGCG on communication with cancer cells and TAM.
methodsMurine breast cancer cell lines, 4T1, was used for in vivo and ex vivo studies. Exosome was extracted from EGCG-treated 4T1 cells, and the change of miRNAs was screened using microarray. Tumor cells or TAM isolated from murine tumor graft were incubated with exosomes derived from EGCG-treated and/or miR-16 inhibitor-transfected 4T1 cells. Chemokines for monocytes (CSF-1 and CCL-2), cytokines both with high (IL-6 and TGF-β) and low (TNF-α) expression in M2 macrophages, and molecules in NF-κB pathway (IKKα and Iκ-B) were evaluated by RT-qPCR or western blot.
resultsEGCG suppressed tumor growth in murine breast cancer model, which was associated with decreased TAM and M2 macrophage infiltration. Expression of chemokine for monocytes (CSF-1 and CCL-2) were low in tumor cells from EGCG-treated mice, and cytokines of TAM was skewed from M2- into M1-like phenotype by EGCG as evidenced by decreased IL-6 and TGF-β and increased TNF-α. Ex vivo incubation of isolated tumor cells with EGCG inhibited the CSF-1 and CCL-2 expression. Ex vivo incubation of TAM with exosomes from EGCG-treated 4T1 cells led to IKKα suppression and concomitant I-κB accumulation; increase of IL-6 and TGF-β; and, decrease of TNF-α. EGCG up-regulated miR-16 in 4T1 cells and in the exosomes. Treatment of tumor cells or TAM with exosomes derived from EGCG-treated and miR-16-knock-downed 4T1 cells restored the above effects on chemokines, cytokines, and NF-κB pathway elicited by EGCG-treated exosomes.
conclusionsOur data demonstrate that EGCG up-regulates miR-16 in tumor cells, which can be transferred to TAM via exosomes and inhibits TAM infiltration and M2 polarization. We suggest a novel mechanism by which EGCG exerts anti-tumor activity via regulation of TAM in tumor microenvironment.
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