Related Experiment Video
Updated: Sep 13, 2025

Polymalic Acid-based Nano Biopolymers for Targeting of Multiple Tumor Markers: An Opportunity for Personalized Medicine?
Published on: June 13, 2014
Decoy Extracellular Vesicles Overcome Triple-Negative Breast Cancer Heterogeneity via Membrane-Cytoplasm-Mitochondria
Chuanrong Chen1, Ming Shen2, Xiaofeng Wan1
1Department of Oncology, Yijishan Hospital of Wannan Medical College, Wuhu, 240001, China.
Abstract:
Triple-negative breast cancer (TNBC) exhibits multilevel heterogeneity, including differences in stemness, immune checkpoint (IC) upregulation, and metabolic plasticity, which has resulted in a lack, of comprehensive treatment strategies. Extracellular vesicles (EVs) from exhausted T cells contain high levels of ICs, which allow them to target and block multiple IC ligands in tumor cells, including cancer stem cells (CSCs). TEAD4 is identified as a pivotal gene facilitating CSC growth and immune escape. Consequently, a novel EV delivery system (siT/MOF@EVs), which targets the tumor cell membrane-cytoplasm-mitochondria cascade, is engineered to codeliver TEAD4-siRNA (siTEAD4) and a mitochondria-targeting metal-organic framework (T/MOF) to overcome tumor heterogeneity. Extracellularly, EVs act as "decoys" by facilitating the binding of IC ligands to target tumor cells, particularly CSCs, and blocking multiple ICs. Within the cytoplasm, the siTEAD4 adsorbed on the T/MOF surface is released, inhibiting CSCs and overcoming immunotherapy resistance. In mitochondria, cascade catalysis by nanozymes that bind monoatomic Pd and Mn2+ triggers an oxidative burst. Additionally, siTEAD4 and T/MOF synergistically block aerobic glycolysis and oxidative phosphorylation and induce immunogenic tumor cell death. siT/MOF@EVs overcome TNBC heterogeneity, inhibit tumor growth and metastasis, and induce protective immune memory in an orthotopic TNBC model without systemic toxicity. Significant therapeutic effects are also observed in a patient-derived organoid xenograft (PDOX) model.
Insights
This study engineered a novel extracellular vesicle (EV) delivery system to target triple-negative breast cancer (TNBC) heterogeneity. The system effectively inhibits cancer stem cells and overcomes immunotherapy resistance, showing significant therapeutic effects.
Area of Science:
- Biomedical Engineering
- Cancer Research
- Immunotherapy
Background:
- Triple-negative breast cancer (TNBC) presents significant heterogeneity, complicating treatment strategies.
- Cancer stem cells (CSCs) and immune checkpoint (IC) upregulation contribute to TNBC's resistance to therapies.
- Extracellular vesicles (EVs) from exhausted T cells can deliver ICs to tumor cells, including CSCs.
Purpose of the Study:
- To develop a novel extracellular vesicle (EV)-based delivery system for overcoming TNBC heterogeneity.
- To simultaneously target cancer stem cells (CSCs) and immune checkpoints (ICs) within TNBC.
- To enhance the efficacy of immunotherapy by addressing metabolic plasticity and immune escape.
Main Methods:
- Engineered a novel EV delivery system (siT/MOF@EVs) to codeliver TEAD4-siRNA (siTEAD4) and a mitochondria-targeting metal-organic framework (T/MOF).
- Utilized EVs as decoys to block IC ligands on tumor cells, particularly CSCs.
- Leveraged nanozymes within mitochondria to trigger oxidative bursts and inhibit tumor metabolism.
Main Results:
- The siT/MOF@EVs system effectively inhibited CSC growth and overcame immunotherapy resistance by delivering siTEAD4.
- Co-delivery of siTEAD4 and T/MOF synergistically blocked tumor aerobic glycolysis and oxidative phosphorylation.
- Demonstrated significant inhibition of tumor growth and metastasis, inducing immunogenic tumor cell death and protective immune memory in TNBC models without systemic toxicity.
Conclusions:
- The engineered siT/MOF@EVs system successfully overcomes TNBC heterogeneity by targeting multiple pathways.
- This novel therapeutic strategy shows potent anti-tumor activity and induces a favorable immune response.
- The findings suggest a promising new approach for treating aggressive triple-negative breast cancer.
Related Concept Videos
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Adaptive Mechanisms in Cancer Cells
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Targeted Cancer Therapies
There are several types of targeted therapies against...

