ArticleInternational journal of oncology2025
Adipocyte‑derived extracellular vesicles sustain mitochondrial metabolism in breast cancer cells: New insights into the cross‑talk between cancer cells and the tumor microenvironment.
Article in International journal of oncology, 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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6 citing papers in PubMed.
- Review
- Cancer-associated adipomes promote invadopodia formation and enhance metastatic potential in triple-negative breast cancer.NPJ breast cancer · 2026Article
- Glycosylated extracellular vesicles drive a metabolic interplay between gastric cancer cells and adipocytes.Extracellular vesicles and circulating nucleic acids · 2026Article
- Adipocyte-derived estrogen signaling influences TROP2 expression in ERα-positive breast cancer.Frontiers in endocrinology · 2026Article
- Immune evasion driven by lipid metabolic reprogramming in endocrine-resistant HRFrontiers in immunology · 2026Review
- Obesity-associated inflammation and cancer: molecular mechanisms, evidence gaps, and therapeutic opportunities.Frontiers in immunology · 2026Review
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Authors and funding
15 authors.
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Abstract
Adipocytes represent the most prominent component of breast tissue stroma and are recognized as significant contributors to the observed association between obesity and breast cancer (BC). It has been widely reported that dysfunctional adipose tissue in obesity has a profound effect on the biology of BC via the secretion of several bioactive molecules. Recently, extracellular vesicles (EVs), a heterogeneous group of membrane‑enclosed structures, have been recognized as key players in adipocyte‑BC cell communication. We previously demonstrated that adipocyte‑derived EVs promoted BC proliferation, migration, invasion, stemness and traits of epithelial‑to‑mesenchymal transition through the activation of hypoxia inducible factor‑1α (HIF‑1α). The present study, to further understand the impact of EVs in breast adiponcosis, investigated the effects of adipocyte‑derived EVs on the BC proteome. By employing liquid chromatography‑tandem mass spectrometry and different bioinformatic tools (such as Proteomap, STRING, FunRich, Reactome and MsigDB), it was found that adipocyte‑derived EVs regulated the expression of multiple proteins implicated in metabolic processes. Adipocyte‑derived EVs shifted cell metabolism towards oxidative phosphorylation in estrogen receptor‑positive (ER+) BC cell lines, including MCF‑7, ZR‑75‑1 and BT‑474 BC cells, through an increased mitochondrial activity along with an enhanced ATP production. These findings were extended by treating BC cells with EVs isolated from the serum of patients with BC classified as normal weight (NW‑EVs) and overweight or obese (OW/Ob‑EVs). Treatment of BC cells with OW/Ob‑EVs resulted in a significant increase of mitochondrial activity and ATP production compared with NW‑EVs. Of note, inhibition of HIF‑1α expression/activity reversed the effects of both adipocyte‑derived EVs and OW/Ob‑EVs on BC cell metabolism. In conclusion, the present study underscored the pivotal role of EVs in the BC‑obesity link, highlighting their involvement in driving metabolic reprogramming in ER+ BC cells through HIF‑1α.
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