Acetylcysteine synergizes PD-1 blockers against colorectal cancer progression by promoting TCF1
Animals
Colorectal Neoplasms
/ pathology
CD8-Positive T-Lymphocytes
/ immunology
Cell Differentiation
/ drug effects
Programmed Cell Death 1 Receptor
/ metabolism
Mice
Acetylcysteine
/ pharmacology
Hepatocyte Nuclear Factor 1-alpha
/ metabolism
Disease Progression
Immune Checkpoint Inhibitors
/ pharmacology
Humans
Cell Line, Tumor
Mice, Inbred C57BL
Drug Synergism
Acetylcysteine
CD8+ T lymphocytes
Colorectal cancer
Glucose transporter 4
PD-1 blockade
Journal
Cell communication and signaling : CCS
ISSN: 1478-811X
Titre abrégé: Cell Commun Signal
Pays: England
ID NLM: 101170464
Informations de publication
Date de publication:
17 Oct 2024
17 Oct 2024
Historique:
received:
22
05
2024
accepted:
23
09
2024
medline:
18
10
2024
pubmed:
18
10
2024
entrez:
17
10
2024
Statut:
epublish
Résumé
Programmed cell death protein 1 (PD-1) blockade is essential in treating progressive colorectal cancer (CRC). However, some patients with CRC do not respond well to immunotherapy, possibly due to the exhaustion of CD8 We constructed a mouse CRC model to study the effect of NAC on tumors. The effect of NAC on CD8 + T cell differentiation and its potential mechanism were explored using cell flow assay and other studies in vitro and ex vivo. We demonstrated that NAC synergized PD-1 antibodies to inhibit CRC progression in a mouse CRC model mediated by CD8 Our study provides a novel idea for immunotherapy for clinically progressive CRC and suggests that Glut4 may be a new immunometabolic molecular target for regulating CD8
Sections du résumé
BACKGROUND
BACKGROUND
Programmed cell death protein 1 (PD-1) blockade is essential in treating progressive colorectal cancer (CRC). However, some patients with CRC do not respond well to immunotherapy, possibly due to the exhaustion of CD8
METHODS
METHODS
We constructed a mouse CRC model to study the effect of NAC on tumors. The effect of NAC on CD8 + T cell differentiation and its potential mechanism were explored using cell flow assay and other studies in vitro and ex vivo.
RESULTS
RESULTS
We demonstrated that NAC synergized PD-1 antibodies to inhibit CRC progression in a mouse CRC model mediated by CD8
CONCLUSIONS
CONCLUSIONS
Our study provides a novel idea for immunotherapy for clinically progressive CRC and suggests that Glut4 may be a new immunometabolic molecular target for regulating CD8
Identifiants
pubmed: 39420342
doi: 10.1186/s12964-024-01848-8
pii: 10.1186/s12964-024-01848-8
doi:
Substances chimiques
Programmed Cell Death 1 Receptor
0
Acetylcysteine
WYQ7N0BPYC
Hepatocyte Nuclear Factor 1-alpha
0
Immune Checkpoint Inhibitors
0
Hnf1a protein, mouse
0
Pdcd1 protein, mouse
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
503Informations de copyright
© 2024. The Author(s).
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