ReviewOncology letters2021
Cross-link between ferroptosis and nasopharyngeal carcinoma: New approach to radiotherapy sensitization.
Review in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- LINC00839 transcriptionally activated by ELK1 represses ferroptosis in nasopharyngeal carcinoma by regulating UPF1/RCHY1/DJ-1 axis.NPJ precision oncology · 2026Article
- Targeting Ferroptosis in Nasopharyngeal Carcinoma: Mechanisms, Resistance, and Precision Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- O-GlcNAc-modified HOXA9 suppresses ferroptosis via promoting UBR5-mediated SIRT6 degradation in nasopharyngeal carcinoma.Neoplasia (New York, N.Y.) · 2025Article
- Differentiating early-stage nasopharyngeal carcinoma from adenoidal hypertrophy via SLC40A1 expression and developing a prognostic model for disease progression.American journal of cancer research · 2025Article
- Article
- The Emerging Role of Ferroptosis in EBV-Associated Cancer: Implications for Cancer Therapy.Biology · 2024Review
- MiR-122-5p regulates erastin-induced ferroptosis via CS in nasopharyngeal carcinoma.Scientific reports · 2024Article
- Berberine-mediated Ferroptosis through System XcJournal of Cancer · 2024Article
- [Icaritin increases radiosensitivity of nasopharyngeal carcinoma cells by regulating iron death].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- ARPC1A is regulated by STAT3 to inhibit ferroptosis and promote prostate cancer progression.Human cell · 2022Article
- Regulation of Ferroptosis by Amino Acid Metabolism in Cancer.International journal of biological sciences · 2022Review
- Ferroptosis regulators related scoring system by Gaussian finite mixture model to predict prognosis and immunotherapy efficacy in nasopharyngeal carcinoma.Frontiers in genetics · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis is a recently discovered special type of regulated cell death that is strongly associated with both homeostasis maintenance and cancer development. Previous studies have indicated that a number of small-molecular agents inducing ferroptosis have great potential in the treatment of different types of cancer, including breast, pancreatic, prostate and head and neck cancer. However, the role of ferroptosis in nasopharyngeal carcinoma (NPC) has remained to be fully determined. To the best of our knowledge, no review of the currently available studies on this subject has been published to date. The metabolism and expression of specific genes that regulate ferroptosis may represent a promising radiosensitization target in cancer treatment. The aim of the present review was to describe the cross-link between ferroptosis and NPC and to discuss the potential value of regulators and the possible mechanism underlying the role of ferroptosis in the radiosensitization of NPC, in the hope that linking the mechanism of ferroptosis with the development of NPC will accelerate the development of novel ferroptosis-based targets and radiotherapy strategies in NPC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.