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Research progress on the regulation of ferroptosis in NPC (Review)

  • Authors:
    • Shuai Bai
    • Yanjie Guo
    • Jingling Qiang
    • Qiangfang Dai
    • Yanling Yang
  • View Affiliations / Copyright

    Affiliations: Department of Neurobiology, School of Basic Medicine, Yan'an Medical College, Yan'an University, Yan'an, Shaanxi 716000, P.R. China, Department of Neurology, Affiliated Hospital of Yan'an University, Yan'an, Shaanxi 716000, P.R. China
    Copyright: © Bai et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 33
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    Published online on: December 18, 2025
       https://doi.org/10.3892/or.2025.9038
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Abstract

Ferroptosis is a novel form of iron‑dependent programmed apoptosis, characterized by dysregulated iron metabolism, impaired antioxidant defense systems and accumulation of lipid peroxidation products. Nasopharyngeal carcinoma (NPC) cells exhibit marked susceptibility to ferroptosis, and its induction can effectively suppress tumor progression, offering a potential therapeutic strategy for NPC. At the molecular level, ferroptosis‑related genes [such as Solute Carrier Family 7 Member 11 (SLC7A11), Glutamate‑Cysteine Ligase Modifier Subunit (GCLM) and Glutamate‑Cysteine Ligase Catalytic Subunit (GCLC)] are notably upregulated in NPC tissues compared with normal tissues, and their overexpression associates with poor patient prognosis, suggesting their utility as diagnostic or prognostic biomarkers. The present review systematically summarizes the molecular mechanisms of ferroptosis, elucidates its role in NPC pathogenesis and discusses ferroptosis‑targeted therapeutic approaches for NPC.
View Figures

Figure 1

Ferroptosis pathway. Schematic
depicts the global ferroptosis regulatory network, integrating
antioxidant systems (such as, GSH-GPX4 and FSP1-CoQ10), iron/lipid
metabolism molecules, MBOAT1/2, and antioxidant/membrane repair
factors to cover key pro- and anti-ferroptosis links. GSH,
glutathione; GSSG, GSH oxide; GPX4, GSH peroxidase 4; GSR, GSH
reductase; FSP1, ferroptosis inhibitory protein 1; CoQ10,
ubiquinone; CoQ10H2, ubiquinol; DHODH, dihydroorotate
dehydrogenase; GTP, phosphohydrolases; GCH1, cyclohydrolase-1; BH2,
dihydrobiopterin; BH4, tetrahydrobiopterin; ACSL4, acyl-CoA
synthetase long-chain family member 4; LOX, lipoxygenase; LPCAT3,
lyso-phosphatidylcholine acyltransferase 3; PUFA, polyunsaturated
fatty acids; CoA, coenzyme A; PL-PUFA, acids-polyunsaturated
polyunsaturated fatty; HO-1, heme oxygenase 1; TRF1, transferrin
receptor; DMT1, divalent metal transporter 1; Keap1, Kelch-like ECH
associated protein 1; MBOAT1/2, o-acyltransferase 1/2; ESCRT,
endosomal sorting complex, required for transport; CHAM5/6, charged
multivesicular proteins 5 and 6; Glu, glutamic acid; PE-PUFA,
unsaturated fat phospholipids; FPN, ferroportin; ARE, antioxidant
response element; Se, Selenium; PL-PUFA-OOH, lipid hydroperoxide;
VK, vitamin K; VKH2, hydroquinone; CoQ10, ubiquinone; CoQ10H2,
ubiquinol; LPLAT, Lys phospholipid acyltransferase.

Figure 2

The ferroptosis pathway associated
with NPC. The schematic illustrates the core ferroptosis regulatory
pathway in NPC, involving the GSH-GPX4 axis,
SLC7A11/SLC3A2-mediated cystine uptake and ROS balance, as well as
the regulatory role of FGF5 secreted by CAFs in the tumor
microenvironment. NPC, nasopharyngeal carcinoma; GSH, glutathione;
GSS, GSH oxide; GPX4, GSH peroxidase 4; SLC7A11, solute carrier
family 7 member 11; SLC3A2, solute carrier family 3 member 2; ROS,
reactive oxygen species; CAFs, cancer-associated fibroblasts; FGF5,
fibroblast growth factor.
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Copy and paste a formatted citation
Spandidos Publications style
Bai S, Guo Y, Qiang J, Dai Q and Yang Y: Research progress on the regulation of ferroptosis in NPC (Review). Oncol Rep 55: 33, 2026.
APA
Bai, S., Guo, Y., Qiang, J., Dai, Q., & Yang, Y. (2026). Research progress on the regulation of ferroptosis in NPC (Review). Oncology Reports, 55, 33. https://doi.org/10.3892/or.2025.9038
MLA
Bai, S., Guo, Y., Qiang, J., Dai, Q., Yang, Y."Research progress on the regulation of ferroptosis in NPC (Review)". Oncology Reports 55.2 (2026): 33.
Chicago
Bai, S., Guo, Y., Qiang, J., Dai, Q., Yang, Y."Research progress on the regulation of ferroptosis in NPC (Review)". Oncology Reports 55, no. 2 (2026): 33. https://doi.org/10.3892/or.2025.9038
Copy and paste a formatted citation
x
Spandidos Publications style
Bai S, Guo Y, Qiang J, Dai Q and Yang Y: Research progress on the regulation of ferroptosis in NPC (Review). Oncol Rep 55: 33, 2026.
APA
Bai, S., Guo, Y., Qiang, J., Dai, Q., & Yang, Y. (2026). Research progress on the regulation of ferroptosis in NPC (Review). Oncology Reports, 55, 33. https://doi.org/10.3892/or.2025.9038
MLA
Bai, S., Guo, Y., Qiang, J., Dai, Q., Yang, Y."Research progress on the regulation of ferroptosis in NPC (Review)". Oncology Reports 55.2 (2026): 33.
Chicago
Bai, S., Guo, Y., Qiang, J., Dai, Q., Yang, Y."Research progress on the regulation of ferroptosis in NPC (Review)". Oncology Reports 55, no. 2 (2026): 33. https://doi.org/10.3892/or.2025.9038
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