Macrophages expedite cell proliferation of prostate intraepithelial neoplasia through their downstream target ERK.
Animals
Antibodies, Neutralizing
/ immunology
Apoptosis
/ drug effects
Cell Line
Cell Proliferation
/ drug effects
Cells, Cultured
Chemokine CCL2
/ metabolism
Cytokines
/ immunology
Humans
Intercellular Adhesion Molecule-1
/ metabolism
MAP Kinase Signaling System
/ drug effects
Macrophages
/ cytology
Male
Mice
Prostatic Intraepithelial Neoplasia
/ metabolism
Prostatic Neoplasms
/ metabolism
RAW 264.7 Cells
C5a
CCL2
cell growth
macrophage
prostate intraepithelial neoplasia
Journal
The FEBS journal
ISSN: 1742-4658
Titre abrégé: FEBS J
Pays: England
ID NLM: 101229646
Informations de publication
Date de publication:
03 2021
03 2021
Historique:
revised:
23
07
2020
received:
20
12
2019
accepted:
24
08
2020
pubmed:
1
9
2020
medline:
28
7
2021
entrez:
1
9
2020
Statut:
ppublish
Résumé
The risk factors for prostate cancer include a high-fat diet and obesity, both of which are associated with an altered cell environment including increased inflammation. It has been shown that chronic inflammation due to a high-fat diet or bacterial infection has the potential to accelerate prostate cancer as well as its precursor, prostatic intraepithelial neoplasia (PIN), development. However, the underlying mechanism of how chronic inflammation promotes prostate cancer development, especially PIN, remains unclear. In this study, we showed that more macrophages were present in PIN areas as compared to the normal areas of human prostate. When co-culturing PIN cells with macrophages in 3D, more PIN cells had nuclear localized cyclin D1, indicating that macrophages enhanced PIN cell proliferation. We identified ICAM-1 and CCL2 as chemoattractants expressed by PIN cells to recruit macrophages. Furthermore, we discovered that macrophage-secreted cytokines including C5a, CXCL1, and CCL2 were responsible for increased PIN cell proliferation. These three cytokines activated ERK and JNK signaling in PIN cells through a ligand-receptor interaction. However, only blockade of ERK abolished macrophage cytokines-induced cell proliferation of PIN. Overall, our results provide a mechanistic view on how macrophages activated through chronic inflammation can expedite PIN progression during prostate cancer development. The information from our work can facilitate a comprehensive understanding of prostate cancer development, which is required for improvement of current strategies for prostate cancer therapy.
Identifiants
pubmed: 32865335
doi: 10.1111/febs.15541
pmc: PMC7914274
mid: NIHMS1630815
doi:
Substances chimiques
Antibodies, Neutralizing
0
Chemokine CCL2
0
Cytokines
0
Intercellular Adhesion Molecule-1
126547-89-5
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
1871-1886Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM103408
Pays : United States
Organisme : NIGMS NIH HHS
ID : P20 GM109095
Pays : United States
Organisme : NIGMS NIH HHS
ID : R25 GM060414
Pays : United States
Organisme : NIMHD NIH HHS
ID : U54 MD007590
Pays : United States
Informations de copyright
© 2020 The Authors. The FEBS Journal published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.
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