High-dose radiation-induced immunogenic cell death of bladder cancer cells leads to dendritic cell activation.
Dendritic Cells
/ immunology
Urinary Bladder Neoplasms
/ immunology
Humans
Cell Line, Tumor
Apoptosis
/ radiation effects
Immunogenic Cell Death
/ radiation effects
Chemokine CCL21
/ metabolism
Receptors, CCR7
/ metabolism
Chemokine CCL5
/ metabolism
Receptors, CCR5
/ metabolism
B7-2 Antigen
/ metabolism
Cell Movement
/ radiation effects
B7-1 Antigen
/ metabolism
Dose-Response Relationship, Radiation
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2024
2024
Historique:
received:
31
01
2024
accepted:
27
06
2024
medline:
4
9
2024
pubmed:
4
9
2024
entrez:
4
9
2024
Statut:
epublish
Résumé
Radiotherapy is a commonly used method in the treatment of bladder cancers (BC). Radiation-induced immunogenic cell death (ICD) is related to the immune response against cancers and their prognoses. Even though dendritic cells (DC) act as powerful antigen-presenting cells in the body, their precise role in this ICD process remains unclear. Accordingly, an in vitro study was undertaken to ascertain whether high-dose radiation-induced ICD of BC cells could regulate the immune response of DC. The results indicated that high-dose radiation treatments of BC cells significantly increased their levels of apoptosis, blocked their cell cycle in the G2/M phase, increased their expression of ICD-related proteins, and upregulated their secretion of CCL5 and CCL21 which control the directed migration of DC. It was also noted that expression of CD80, CD86, CCR5, and CCR7 on DC was upregulated in the medium containing the irradiated cells. In conclusion, the present findings illustrate that high-dose radiation can induce the occurrence of ICD within BC cells, concomitantly resulting in the activation of DC. Such findings could be of great significance in increasing the understanding how radiotherapy of BC may work to bring about reductions in cell activity and how these processes in turn lead to immunoregulation of the function of DC.
Identifiants
pubmed: 39231199
doi: 10.1371/journal.pone.0307024
pii: PONE-D-24-01224
doi:
Substances chimiques
Chemokine CCL21
0
Receptors, CCR7
0
Chemokine CCL5
0
CCL21 protein, human
0
Receptors, CCR5
0
CCR7 protein, human
0
B7-2 Antigen
0
CCL5 protein, human
0
CCR5 protein, human
0
B7-1 Antigen
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0307024Informations de copyright
Copyright: © 2024 Zeng et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.