ArticlePloS one2024
CAPE activates AMPK and Foxo3 signaling to induce growth inhibition and ferroptosis in triple-negative breast cancer.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Ferroptosis in breast cancer: From adipocyte-immune-iron regulation to therapeutic application.Clinical and translational medicine · 2026Review
- PTK6 suppresses NSCLC ferroptosis by promoting m6A-YTHDF2-dependent FOXO3 mRNA degradation through phosphorylation.Molecular genetics and genomics : MGG · 2026Article
- EVA1A-Mediated Signaling Networks in Physiological and Pathological Contexts: Dual Roles in Autophagy and Apoptosis.Cell biochemistry and biophysics · 2026Review
- Co-targeting ferroptosis and immune evasion through small molecules in breast cancer.Journal of translational internal medicine · 2025Article
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Authors and funding
5 authors.
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Abstract
purposeApproximately 20% of all breast cancer cases are classified as triple-negative breast cancer (TNBC), which represents the most challenging subtype due to its poor prognosis and high metastatic rate. Caffeic acid phenethyl ester (CAPE), the main component extracted from propolis, has been reported to exhibit anticancer activity across various tumor cell types. This study aimed to investigate the effects and mechanisms of CAPE on TNBC.
methodsMDA-MB-231 and MDA-MB-468 cells were treated with CAPE. CCK8 and colony formation assays were performed to analyze cell proliferation. Western blot, TUNEL and Annexin V-FITC/PI staining methods were employed to assess cell apoptosis. ROS, MDA, SOD, GSH, C11-bodipy staining, along with measurements of GPX4 and Ferritin levels, were utilized for ferroptosis detection. Western blot and immunofluorescence analysis were used to assess key regulatory molecules. The cells were subjected to treatments involving ferroptosis inhibition, AMPK inhibition, or Foxo3 inhibition, followed by CAPE administration to assess cell proliferation, apoptosis, and ferroptosis. Tumor xenografts were used to evaluate the antitumor efficacy of CAPE.
resultsCAPE not only suppressed cell proliferation but also promoted apoptosis followed by ferroptosis. Co-incubation with Fer-1 (a ferroptosis inhibitor) diminished CAPE's suppressive effects on proliferation and apoptosis induction. CAPE treatment enhanced the phosphorylation of AMPK and promoted the nuclear translocation of Foxo3. Inhibition of both AMPK and Foxo3 by siRNAs or inhibitors (Compc, TIC10) reversed the growth retardation induced by CAPE as well as its pro-apoptotic effects leading to ferroptosis. Specifically, AMPK inhibition abrogated the CAPE-induced nuclear translocation of Foxo3. CAPE significantly inhibited tumor growth in nude mice bearing TNBC xenografts.
conclusionCAPE possesses a resistance effect on TNBC via activation of AMPK and Foxo3 signaling pathways.
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