ArticleJournal of extracellular vesicles2024
Baohuoside I chemosensitises breast cancer to paclitaxel by suppressing extracellular vesicle/CXCL1 signal released from apoptotic cells.
Article in Journal of extracellular vesicles, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The trial behind it
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Who cites it
18 citing papers in PubMed.
- GTPase RAB31 supports ANXA1-driven macrophage education through clathrin-mediated endocytosis to suppress antitumor immunity.Journal for immunotherapy of cancer · 2026Article
- Tumor-derived apoptotic extracellular vesicles impede hepatocarcinoma progression by disrupting mitochondrial metabolism.Journal of translational medicine · 2026Article
- The Multifaceted Role of Extracellular Vesicles in Triple Negative Breast Cancer.International journal of molecular sciences · 2026Review
- CXCL1 in triple‑negative breast cancer: Mechanisms, challenges, and therapeutic opportunities (Review).Oncology reports · 2026Review
- Ginkgetin enhances the antitumor effect of Taxol on human breast cancer MCF-7 cells via ferroptosis mediated by the MDM2-p53-YAP1 axis.Scientific reports · 2026Article
- Targeting tumor-associated macrophages through phytochemicals: a promising strategy for cold tumor therapy.Chinese medicine · 2026Review
- Apoptotic vesicles: from biological characteristics to clinical translational prospects.Journal of translational medicine · 2026Review
- Remodeling the tumor immune microenvironment: mechanisms of crosstalk between regulated cell death macrophages.Frontiers in immunology · 2026Review
- Molecular innate immune programs of tumor-associated macrophages in immune checkpoint blockade resistance: a staged framework from suppressive circuitry to translational bottlenecks.Frontiers in immunology · 2026Review
- Natural Combatants: How Herbal Monomers Regulate Autophagy in Ovarian Cancer.Anti-cancer agents in medicinal chemistry · 2026Review
- Macrophage-cancer cell crosstalk in breast cancer chemotherapy resistance.Medical oncology (Northwood, London, England) · 2025Review
- LSD1 inhibition sensitizes anti-PD1 blockade immunotherapy by inhibiting the long-range attack of tumor-derived extracellular vesicles.Acta pharmaceutica Sinica. B · 2025Article
- Engineered Extracellular Vesicles for Targeted Paclitaxel Delivery in Cancer Therapy: Advances, Challenges, and Prospects.Cellular and molecular bioengineering · 2025Review
- Targeting Resistance Pathways in Breast Cancer Through Precision Oncology: Nanotechnology and Immune Modulation Approaches.Biomedicines · 2025Review
- Curcumenol inhibits malignant progression and promotes ferroptosis via the SLC7A11/NF‑κB/TGF‑β pathway in triple‑negative breast cancer.International journal of molecular medicine · 2025Article
- Review
- Tumor-derived extracellular vesicles: key drivers of immunomodulation in breast cancer.Frontiers in immunology · 2025Review
- Baohuoside I chemosensitises breast cancer to paclitaxel by suppressing extracellular vesicle/CXCL1 signal released from apoptotic cells.Journal of extracellular vesicles · 2024Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype and chemotherapy is the cornerstone treatment for TNBC. Regrettably, emerging findings suggest that chemotherapy facilitates pro-metastatic changes in the tumour microenvironment. Extracellular vesicles (EVs) have been highly implicated in cancer drug resistance and metastasis. However, the effects of the EVs released from dying cancer cells on TNBC prognosis and corresponding therapeutic strategies have been poorly investigated. This study demonstrated that paclitaxel chemotherapy elicited CXCL1-enriched EVs from apoptotic TNBC cells (EV-Apo). EV-Apo promoted the chemoresistance and invasion of co-cultured TNBC cells by polarizing M2 macrophages through activating PD-L1 signalling. However, baohuoside I (BHS) remarkably sensitized the co-cultured TNBC cells to paclitaxel chemotherapy via modulating EV-Apo signalling. Mechanistically, BHS remarkably decreased C-X-C motif chemokine ligand 1 (CXCL1) cargo within EV-Apo and therefore attenuated macrophage M2 polarization by suppressing PD-L1 activation. Additionally, BHS decreased EV-Apo release by diminishing the biogenesis of intraluminal vesicles (ILVs) within multivesicular bodies (MVBs) of TNBC cells. Furthermore, BHS bound to the LEU104 residue of flotillin 2 (FLOT2) and interrupted its interaction with RAS oncogene family member 31 (RAB31), leading to the blockage of RAB31-FLOT2 complex-driven ILV biogenesis. Importantly, BHS remarkably chemosensitised paclitaxel to inhibit TNBC metastasis in vivo by suppressing EV-Apo
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