Crosstalk between tumour and stroma modifies CLIC4 cargo in extracellular vesicles
Abstract Mouse models of breast cancer have revealed that tumour‐bearing hosts must express the oxidoreductase CLIC4 to develop lung metastases. In the absence of host CLIC4, primary tumours grow but the lung premetastatic niche is defective for metastatic seeding. Primary breast cancer cells releas...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2023-10-01
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| Series: | Journal of Extracellular Biology |
| Subjects: | |
| Online Access: | https://doi.org/10.1002/jex2.118 |
| _version_ | 1797654535132413952 |
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| author | Vanesa C. Sanchez Alayna Craig‐Lucas Christophe Cataisson Brandi L. Carofino Stuart H. Yuspa |
| author_facet | Vanesa C. Sanchez Alayna Craig‐Lucas Christophe Cataisson Brandi L. Carofino Stuart H. Yuspa |
| author_sort | Vanesa C. Sanchez |
| collection | DOAJ |
| description | Abstract Mouse models of breast cancer have revealed that tumour‐bearing hosts must express the oxidoreductase CLIC4 to develop lung metastases. In the absence of host CLIC4, primary tumours grow but the lung premetastatic niche is defective for metastatic seeding. Primary breast cancer cells release EVs that incorporate CLIC4 as cargo and circulate in plasma of wildtype tumour‐bearing hosts. CLIC4‐deficient breast cancer cells also form tumours in wildtype hosts and release EVs in plasma, but these EVs lack CLIC4, suggesting that the tumour is the source of the plasma‐derived EVs that carry CLIC4 as cargo. Paradoxically, circulating EVs are also devoid of CLIC4 when CLIC4‐expressing primary tumours are grown in CLIC4 knockout hosts. Thus, the incorporation of CLIC4 (and perhaps other factors) as EV cargo released from tumours involve specific signals from the surrounding stroma determined by its genetic composition. Since CLIC4 is also detected in circulating EVs from human breast cancer patients, future studies will address its association with disease. |
| first_indexed | 2024-03-11T17:00:53Z |
| format | Article |
| id | doaj.art-ff75b39973fb4ceda5f966035cbeeddc |
| institution | Directory Open Access Journal |
| issn | 2768-2811 |
| language | English |
| last_indexed | 2024-03-11T17:00:53Z |
| publishDate | 2023-10-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Extracellular Biology |
| spelling | doaj.art-ff75b39973fb4ceda5f966035cbeeddc2023-10-20T10:40:29ZengWileyJournal of Extracellular Biology2768-28112023-10-01210n/an/a10.1002/jex2.118Crosstalk between tumour and stroma modifies CLIC4 cargo in extracellular vesiclesVanesa C. Sanchez0Alayna Craig‐Lucas1Christophe Cataisson2Brandi L. Carofino3Stuart H. Yuspa4Center for Drug Evaluation and Research U.S. Food and Drug Administration Silver Spring Maryland USADepartment of Surgery Lehigh Valley Health Network Allentown Pennsylvania USALaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute National Institutes of Health Bethesda Maryland USALaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute National Institutes of Health Bethesda Maryland USALaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute National Institutes of Health Bethesda Maryland USAAbstract Mouse models of breast cancer have revealed that tumour‐bearing hosts must express the oxidoreductase CLIC4 to develop lung metastases. In the absence of host CLIC4, primary tumours grow but the lung premetastatic niche is defective for metastatic seeding. Primary breast cancer cells release EVs that incorporate CLIC4 as cargo and circulate in plasma of wildtype tumour‐bearing hosts. CLIC4‐deficient breast cancer cells also form tumours in wildtype hosts and release EVs in plasma, but these EVs lack CLIC4, suggesting that the tumour is the source of the plasma‐derived EVs that carry CLIC4 as cargo. Paradoxically, circulating EVs are also devoid of CLIC4 when CLIC4‐expressing primary tumours are grown in CLIC4 knockout hosts. Thus, the incorporation of CLIC4 (and perhaps other factors) as EV cargo released from tumours involve specific signals from the surrounding stroma determined by its genetic composition. Since CLIC4 is also detected in circulating EVs from human breast cancer patients, future studies will address its association with disease.https://doi.org/10.1002/jex2.118breast cancerCLIC4exosomestumour‐stromal interaction |
| spellingShingle | Vanesa C. Sanchez Alayna Craig‐Lucas Christophe Cataisson Brandi L. Carofino Stuart H. Yuspa Crosstalk between tumour and stroma modifies CLIC4 cargo in extracellular vesicles Journal of Extracellular Biology breast cancer CLIC4 exosomes tumour‐stromal interaction |
| title | Crosstalk between tumour and stroma modifies CLIC4 cargo in extracellular vesicles |
| title_full | Crosstalk between tumour and stroma modifies CLIC4 cargo in extracellular vesicles |
| title_fullStr | Crosstalk between tumour and stroma modifies CLIC4 cargo in extracellular vesicles |
| title_full_unstemmed | Crosstalk between tumour and stroma modifies CLIC4 cargo in extracellular vesicles |
| title_short | Crosstalk between tumour and stroma modifies CLIC4 cargo in extracellular vesicles |
| title_sort | crosstalk between tumour and stroma modifies clic4 cargo in extracellular vesicles |
| topic | breast cancer CLIC4 exosomes tumour‐stromal interaction |
| url | https://doi.org/10.1002/jex2.118 |
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