1. ACT001 inhibits primary central nervous system lymphoma tumor growth by enhancing the anti-tumor effect of T cells.
- Author
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Liu Z, Wang G, Liu H, Ding K, Song J, and Fu R
- Subjects
- Animals, Cell Line, Tumor, Mice, Humans, B7-H1 Antigen metabolism, Mice, Inbred NOD, Programmed Cell Death 1 Receptor antagonists & inhibitors, Antineoplastic Agents pharmacology, Xenograft Model Antitumor Assays, Cell Proliferation drug effects, T-Lymphocytes drug effects, T-Lymphocytes immunology, Apoptosis drug effects, Central Nervous System Neoplasms drug therapy, Central Nervous System Neoplasms pathology, Central Nervous System Neoplasms immunology, Lymphoma drug therapy, Lymphoma pathology, Lymphoma immunology
- Abstract
Primary central nervous system lymphoma (PCNSL) is a group of malignant brain tumors with a poor prognosis, and new therapeutic approaches for this tumor urgently need to be investigated. Formulated from a long-standing anti-inflammatory drugs, ACT001 has demonstrated in clinical research to be able to pass through the blood-brain barrier (BBB) and affect the central nervous system. The effects of ACT001 on PCNSL cell apoptosis, proliferation and immune-related indexes were detected by flow cytometry, and the efficacy of ACT001 was verified in vivo by constructing a mouse PCNSL tumor model. ACT001 significantly inhibited PCNSL cell proliferation and induced apoptosis in vitro. In addition, ACT001 can significantly inhibit the PD-1/PD-L1 expression and restore the function of T cells, so that the immune system cannot allow tumor cells to escape. In vivo experiments show that co-infusion of ACT001 and T cells effectively inhibits PCNSL tumor growth in NSG mice. Our work describes the inhibitory effect of ACT001 on the PCNSL cell line and demonstrated the inhibitory effect of ACT001 on immune checkpoints., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Masson SAS.)
- Published
- 2024
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