Activated platelets facilitate hematogenous metastasis of breast cancer by modulating the PDGFR-β/COX-2 axis.
Cancer
Cellular physiology
Molecular biology
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
15 Sep 2023
15 Sep 2023
Historique:
received:
24
05
2023
revised:
03
07
2023
accepted:
21
08
2023
medline:
8
9
2023
pubmed:
8
9
2023
entrez:
8
9
2023
Statut:
epublish
Résumé
Platelets have been widely recognized as a bona fide mediator of malignant diseases, and they play significant roles in influencing various aspects of tumor progression. Paracrine interactions between platelets and tumor cells have been implicated in promoting the dissemination of malignant cells to distant sites. However, the underlying mechanisms of the platelet-tumor cell interactions for promoting hematogenous metastasis are not yet fully understood. We found that activated platelets with high expression of CD36 were prone to release a plethora of growth factors and cytokines, including high levels of PDGF-B, compared to resting platelets. PDGF-B activated the PDGFR-β/COX-2 signaling cascade, which elevated an array of pro-inflammatory factors levels, thereby aggravating tumor metastasis. The collective administration of CD36 inhibitor and COX-2 inhibitor resolved the interactions between platelets and tumor cells. Collectively, our findings demonstrated that targeting the crosstalk between platelets and tumor cells offers potential therapeutic strategies for inhibiting tumor metastasis.
Identifiants
pubmed: 37680480
doi: 10.1016/j.isci.2023.107704
pii: S2589-0042(23)01781-9
pmc: PMC10480622
doi:
Types de publication
Journal Article
Langues
eng
Pagination
107704Informations de copyright
© 2023 The Author(s).
Déclaration de conflit d'intérêts
The authors declare that they have no competing interest that could have appeared to influence the work reported in this paper.
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