Spindle pole body component 25 and platelet-derived growth factor mediate crosstalk between tumor-associated macrophages and prostate cancer cells.
Cell Line, Tumor
Humans
Male
Microtubule-Associated Proteins
/ metabolism
Platelet-Derived Growth Factor
/ metabolism
Prostate
/ metabolism
Prostatic Neoplasms
/ metabolism
Receptor Cross-Talk
/ physiology
Receptors, Platelet-Derived Growth Factor
/ metabolism
Signal Transduction
Spindle Pole Bodies
/ metabolism
Transforming Growth Factor beta1
/ metabolism
Tumor Microenvironment
Tumor-Associated Macrophages
/ metabolism
SPC25
crosstalk
pdgf
prostate cancer
tumor associated macrophage (TAM)
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2022
2022
Historique:
received:
01
04
2022
accepted:
05
07
2022
entrez:
15
8
2022
pubmed:
16
8
2022
medline:
17
8
2022
Statut:
epublish
Résumé
Tumor-associated macrophages (TAMs) are involved in the growth of prostate cancer (PrC), while the molecular mechanisms underlying the interactive crosstalk between TAM and PrC cells remain largely unknown. Platelet-derived growth factor (PDGF) is known to promote mesenchymal stromal cell chemotaxis to the tumor microenvironment. Recently, activation of spindle pole body component 25 (SPC25) has been shown to promote PrC cell proliferation and is associated with PrC stemness. Here, the relationship between SPC25 and PDGF in the crosstalk between TAM and PrC was investigated. Significant increases in both PDGF and SPC25 levels were detected in PrC specimens compared to paired adjacent normal prostate tissues. A significant correlation was detected between PDGF and SPC25 levels in PrC specimens and cell lines. SPC25 increased PDGF production and tumor cell growth in cultured PrC cells and in xenotransplantation. Mechanistically, SPC25 appeared to activate PDGF in PrC likely through Early Growth Response 1 (Egr1), while the secreted PDGF signaled to TAM through PDGFR on macrophages and polarized macrophages, which, in turn, induced the growth of PrC cells likely through their production and secretion of transforming growth factor β1 (TGFβ1). Thus, our data suggest that SPC25 triggers the crosstalk between TAM and PrC cells
Identifiants
pubmed: 35967419
doi: 10.3389/fimmu.2022.907636
pmc: PMC9363606
doi:
Substances chimiques
Microtubule-Associated Proteins
0
Platelet-Derived Growth Factor
0
SPC25 protein, human
0
TGFB1 protein, human
0
Transforming Growth Factor beta1
0
Receptors, Platelet-Derived Growth Factor
EC 2.7.10.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
907636Informations de copyright
Copyright © 2022 Cui, Xu, Hu and Lv.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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