ArticleInternational journal of oncology2018
High COX-2 expression contributes to a poor prognosis through the inhibition of chemotherapy-induced senescence in nasopharyngeal carcinoma.
Article in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Bevacizumab enhances overall survival in newly diagnosed glioblastoma patients with high COX-2 expression.Scientific reports · 2026Article
- The COX-2 Inhibitor Celecoxib Sensitizes Nasopharyngeal Carcinoma Cells to Ferroptosis.Current cancer drug targets · 2026Article
- Advanced hierarchical computational modeling-based rational development of platinum (II) nanocomplex to improve lung cancer therapy.Advanced functional materials · 2025Article
- Article
- An In Vitro Examination of Whether Kratom Extracts Enhance the Cytotoxicity of Low-Dose Doxorubicin against A549 Human Lung Cancer Cells.Molecules (Basel, Switzerland) · 2024Article
- Precision medicine in nasopharyngeal carcinoma: comprehensive review of past, present, and future prospect.Journal of translational medicine · 2023Review
- Lipocalin 2 Reduces MET Levels by Inhibiting MEK/ERK Signaling to Inhibit Nasopharyngeal Carcinoma Cell Migration.Cancers · 2022Article
- Activation and Evasion of Innate Immunity by Gammaherpesviruses.Journal of molecular biology · 2022Review
- Prognostic Impact of Indicators of Systemic Inflammation and the Nutritional Status of Patients with Resected Carcinoma of the Ampulla of Vater: A Single-Center Retrospective Study.World journal of surgery · 2022Article
- Potential Molecular Mechanism of Upregulated Aryl Hydrocarbon Receptor Nuclear Translocator 2 in Nasopharyngeal Carcinoma.Computational and mathematical methods in medicine · 2022Article
- Cyclooxygenase-2 expression is associated with chemoresistance through cancer stemness property in hypopharyngeal carcinoma.Oncology letters · 2021Article
- COX2 confers bone marrow stromal cells to promoting TNFα/TNFR1β-mediated myeloma cell growth and adhesion.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Tumor microenvironment and radioresistance.Experimental & molecular medicine · 2021Review
- Cyclooxygenase-2 induces neoplastic transformation by inhibiting p53-dependent oncogene-induced senescence.Scientific reports · 2021Article
- A Gene-Expression Predictor for Efficacy of Induction Chemotherapy in Locoregionally Advanced Nasopharyngeal Carcinoma.Journal of the National Cancer Institute · 2021Article
- A novel immunochemotherapy based on targeting of cyclooxygenase and induction of immunogenic cell death.Biomaterials · 2021Article
- Transcriptomic Analyses Reveal Gene Expression Profiles and Networks in Nasopharyngeal Carcinoma.BioMed research international · 2021Article
- Advances in targeted therapy mainly based on signal pathways for nasopharyngeal carcinoma.Signal transduction and targeted therapy · 2020Review
- High COX-2 expression in cancer-associated fibiroblasts contributes to poor survival and promotes migration and invasiveness in nasopharyngeal carcinoma.Molecular carcinogenesis · 2020Article
- Influence of perioperative anaesthetic and analgesic interventions on oncological outcomes: a narrative review.British journal of anaesthesia · 2019Review
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance to radiotherapy and chemotherapy currently represents one of the major reasons for therapeutic failure in nasopharyngeal carcinoma (NPC). However, the mechanisms underlying resistance to chemotherapy in NPC remain unclear. In this study, cell counting assay, cell cycle assay and senescence associated β-galactosidase activity were performed to evaluate cell growth, proliferation and senescence, respectively. We found that the aberrant expression of cyclooxygenase-2 (COX-2) was associated with a poor outcome and recurrance in patients with NPC. In NPC cells, COX-2 overexpression increased cell proliferation, inhibited cellular senescence and resulted in chemoresistance, while the knockdown of COX-2 reduced cell proliferation, promoted cellular senescence and overcame chemoresistance. Furthermore, fibroblasts from COX-2 knockout mice exhibited cellular senescence, particularly when treated with chemotherapeutic agents. Mechanistically, COX-2 interacted with p53 protein and inhibited cellular senescence, which resulted in chemotherapeutic resistance. On the whole, these findings indicate that COX-2 may play a critical role in chemotherapeutic resistance in NPC via the inhibition of chemotherapy-induced senescence via the inactivation of p53. This study provides experimental evidence for the preclinical value of increasing chemotherapy-induced senescence by targeting COX-2 as an effective antitumor treatment in patients with recurrent NPC.
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