ArticleFrontiers in oncology2025
Capsaicin induces ferroptosis via suppression of SLC7A11 activity and upregulation of ACSL4 mediated by AMPK in tongue squamous cell carcinoma.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Targeting SLC7A11 with Chinese Medicine for Tumor Ferroptosis Induction: From Molecular Mechanisms to Novel Precision Therapeutic Strategies.Chinese journal of integrative medicine · 2026Review
- The AMPK-BECN1-System Xc⁻ Pathway in Traumatic Brain Injury: Implications for Exosome-Based Therapy.Cellular and molecular neurobiology · 2026Review
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9 authors.
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Abstract
Introduction: The global incidence of tongue squamous cell carcinoma (TSCC) has been steadily increasing. Our previous studies have demonstrated that capsaicin (CAP) promotes apoptosis and inhibits cell migration, thereby exerting anti-TSCC effects. In this study, we aimed to validate whether CAP induces ferroptosis in TSCC and to elucidate the underlying mechanisms. Methods: Cell viability in HN6 and CAL27 cells was assessed using CCK-8 assays. Mitochondrial structural changes were observed via transmission electron microscopy (TEM). The levels of malondialdehyde (MDA), Fe Results: CAP significantly suppressed the viability of HN6 and CAL27 cells. TEM analysis revealed mitochondrial damage following CAP treatment. Furthermore, CAP increased levels of MDA, Fe²⁺, and ROS while decreasing GSH; these alterations were reversed by Fer-1 treatment. Western blot analyses indicated that CAP upregulated phosphorylated AMPK and ACSL4 but downregulated GPX4 expression. Moreover, CAP inhibited glutamate release while enhancing BECN1-SLC7A11 binding, suggesting a reduction in SLC7A11 activity through the AMPK/BECN1 pathway. Notably, AMPK inhibition mitigated CAP-induced changes in p-BECN1, ACSL4, MDA, Fe²⁺, GSH, and ROS levels. Discussion: Our study demonstrates that CAP activate the AMPK signaling, inhibits the activity of SLC7A11 and increases ACSL4 expression, thereby inducing ferroptosis in TSCC. These findings, supported by
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