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Publication : Coagulation factor X promotes resistance to androgen-deprivation therapy in prostate cancer.

First Author	Calì B	Year	2024
Journal	Cancer Cell	Volume	42
Issue	10	Pages	1676-1692.e11
PubMed ID	39303726	Mgi Jnum	J:357411
Mgi Id	MGI:7763524	Doi	10.1016/j.ccell.2024.08.018
Citation	Cali B, et al. (2024) Coagulation factor X promotes resistance to androgen-deprivation therapy in prostate cancer. Cancer Cell 42(10):1676-1692.e11

abstractText

Although hypercoagulability is commonly associated with malignancies, whether coagulation factors directly affect tumor cell proliferation remains unclear. Herein, by performing single-cell RNA sequencing (scRNA-seq) of the prostate tumor microenvironment (TME) of mouse models of castration-resistant prostate cancer (CRPC), we report that immunosuppressive neutrophils (PMN-MDSCs) are a key extra-hepatic source of coagulation factor X (FX). FX activation within the TME enhances androgen-independent tumor growth by activating the protease-activated receptor 2 (PAR2) and the phosphorylation of ERK1/2 in tumor cells. Genetic and pharmacological inhibition of factor Xa (FXa) antagonizes the oncogenic activity of PMN-MDSCs, reduces tumor progression, and synergizes with enzalutamide therapy. Intriguingly, F10(high) PMN-MDSCs express the surface marker CD84 and CD84 ligation enhances F10 expression. Elevated levels of FX, CD84, and PAR2 in prostate tumors associate with worse survival in CRPC patients. This study provides evidence that FXa directly promotes cancer and highlights additional targets for PMN-MDSCs for cancer therapies.

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