ArticleOxidative medicine and cellular longevity2022
Capecitabine Regulates HSP90AB1 Expression and Induces Apoptosis via Akt/SMARCC1/AP-1/ROS Axis in T Cells.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Transcriptional and functional profiling reveals unique activation of Adapter CAR T cells in acute myeloid leukemia.Journal of translational medicine · 2026Article
- Melatonin and cerium oxide nanoparticles additively mitigate capecitabine-induced hepatotoxicity via targeting oxidative stress, apoptosis, and ERK signaling.BMC pharmacology & toxicology · 2026Article
- The distinct roles of ROS in tumor immunity: from mechanisms to immunotherapeutic applications.Journal of hematology & oncology · 2026Review
- TBKBP1 induces capecitabine resistance through negative regulation of type I interferon pathway in triple-negative breast cancer.Oncogene · 2026Article
- Article
- Ginkgolic acid inhibits CD8Journal of pharmaceutical analysis · 2025Article
- Proteomics Reveals the Response Mechanism of Embryonic Bovine Lung Cells toInternational journal of molecular sciences · 2025Article
- CD226 implicated in Akt-dependent apoptosis of CD4Cell death & disease · 2024Article
- Transplant oncology and anti-cancer immunosuppressants.Frontiers in immunology · 2024Review
- Aberrant Expressions ofCurrent genomics · 2023Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transplant oncology is a newly emerging discipline integrating oncology, transplant medicine, and surgery and has brought malignancy treatment into a new era via transplantation. In this context, obtaining a drug with both immunosuppressive and antitumor effects can take into account the dual needs of preventing both transplant rejection and tumor recurrence in liver transplantation patients with malignancies. Capecitabine (CAP), a classic antitumor drug, has been shown to induce reactive oxygen species (ROS) production and apoptosis in tumor cells. Meanwhile, we have demonstrated that CAP can induce ROS production and apoptosis in T cells to exert immunosuppressive effects, but its underlying molecular mechanism is still unclear. In this study, metronomic doses of CAP were administered to normal mice by gavage, and the spleen was selected for quantitative proteomic and phosphoproteomic analysis. The results showed that CAP significantly reduced the expression of HSP90AB1 and SMARCC1 in the spleen. It was subsequently confirmed that CAP also significantly reduced the expression of HSP90AB1 and SMARCC1 and increased ROS and apoptosis levels in T cells. The results of in vitro experiments showed that HSP90AB1 knockdown resulted in a significant decrease in
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