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The CD151-midkine pathway regulates the immune microenvironment in inflammatory breast cancer
S. Hayward, M. Gachehiladze, N. Badr, R. Andrijes, G. Molostvov, L. Paniushkina, B. Sopikova, Z. Slobodová, G. Mgebrishvili, N. Sharma, Y. Horimoto, D. Burg, G. Robertson, A. Hanby, F. Hoar, D. Rea, BL. Eckhardt, NT. Ueno, I. Nazarenko, HM. Long,...
Jazyk angličtina Země Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
32129471
DOI
10.1002/path.5415
Knihovny.cz E-zdroje
- MeSH
- antigeny CD151 imunologie metabolismus MeSH
- chemokiny metabolismus MeSH
- lidé MeSH
- makrofágy metabolismus patologie MeSH
- midkin metabolismus MeSH
- nádorové buněčné linie MeSH
- nádorové mikroprostředí fyziologie MeSH
- zánětlivé nádory prsu metabolismus patologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
The immune microenvironment in inflammatory breast cancer (IBC) is poorly characterised, and molecular and cellular pathways that control accumulation of various immune cells in IBC tissues remain largely unknown. Here, we discovered a novel pathway linking the expression of the tetraspanin protein CD151 in tumour cells with increased accumulation of macrophages in cancerous tissues. It is notable that elevated expression of CD151 and a higher number of tumour-infiltrating macrophages correlated with better patient responses to chemotherapy. Accordingly, CD151-expressing IBC xenografts were characterised by the increased infiltration of macrophages. In vitro migration experiments demonstrated that CD151 stimulates the chemoattractive potential of IBC cells for monocytes via mechanisms involving midkine (a heparin-binding growth factor), integrin α6β1, and production of extracellular vesicles (EVs). Profiling of chemokines secreted by IBC cells demonstrated that CD151 increases production of midkine. Purified midkine specifically stimulated migration of monocytes, but not other immune cells. Further experiments demonstrated that the chemoattractive potential of IBC-derived EVs is blocked by anti-midkine antibodies. These results demonstrate for the first time that changes in the expression of a tetraspanin protein by tumour cells can affect the formation of the immune microenvironment by modulating recruitment of effector cells to cancerous tissues. Therefore, a CD151-midkine pathway can be considered as a novel target for controlled changes of the immune landscape in IBC. © 2020 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Breast Unit St James Hospital Leeds Teaching Hospitals NHS Trust Leeds UK
Department of Breast Surgical Oncology Juntendo University School of Medicine Tokyo Japan
Department of Clinical and Molecular Pathology Palacký Univerzity Olomouc Czech Republic
Institute of Cancer and Genomic Sciences The University of Birmingham Birmingham UK
University of Leeds Leeds Institute of Cancer and Pathology Leeds Leeds UK
Citace poskytuje Crossref.org
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- $a The immune microenvironment in inflammatory breast cancer (IBC) is poorly characterised, and molecular and cellular pathways that control accumulation of various immune cells in IBC tissues remain largely unknown. Here, we discovered a novel pathway linking the expression of the tetraspanin protein CD151 in tumour cells with increased accumulation of macrophages in cancerous tissues. It is notable that elevated expression of CD151 and a higher number of tumour-infiltrating macrophages correlated with better patient responses to chemotherapy. Accordingly, CD151-expressing IBC xenografts were characterised by the increased infiltration of macrophages. In vitro migration experiments demonstrated that CD151 stimulates the chemoattractive potential of IBC cells for monocytes via mechanisms involving midkine (a heparin-binding growth factor), integrin α6β1, and production of extracellular vesicles (EVs). Profiling of chemokines secreted by IBC cells demonstrated that CD151 increases production of midkine. Purified midkine specifically stimulated migration of monocytes, but not other immune cells. Further experiments demonstrated that the chemoattractive potential of IBC-derived EVs is blocked by anti-midkine antibodies. These results demonstrate for the first time that changes in the expression of a tetraspanin protein by tumour cells can affect the formation of the immune microenvironment by modulating recruitment of effector cells to cancerous tissues. Therefore, a CD151-midkine pathway can be considered as a novel target for controlled changes of the immune landscape in IBC. © 2020 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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