ArticleCell communication and signaling : CCS2024
Acetylcysteine synergizes PD-1 blockers against colorectal cancer progression by promoting TCF1
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Metabolic heterogeneity and functional diversity of cancer-associated fibroblasts in gastric cancer (Review).Oncology letters · 2026Review
- Article
- Breathing new life into T-cell receptor-engineered T-cell therapy in solid tumors: enhancing strategies to expand the universality of precision therapy.Experimental hematology & oncology · 2026Review
- Redefining the role of the thiol-based agentRSC medicinal chemistry · 2026Review
- Potential treatment benefits of a GLP-1R antagonist in combination with immune checkpoint inhibitors in colorectal cancer.Oncology letters · 2026Article
- Revitalizing T cells: breakthroughs and challenges in overcoming T cell exhaustion.Signal transduction and targeted therapy · 2026Review
- Effects of functional antioxidants on the expansion of gamma delta T-cells and their cellular cytotoxicity against bladder cancer cells.BMC cancer · 2025Article
- N-Acetyl Cysteine as a promising therapeutic approach in ovarian cancer: potential and perspectives.Academia oncology · 2025Article
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Authors and funding
10 authors.
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Abstract
backgroundProgrammed 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
methodsWe 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.
resultsWe demonstrated that NAC synergized PD-1 antibodies to inhibit CRC progression in a mouse CRC model mediated by CD8
conclusionsOur 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
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