ArticleJournal of oncology2021
Ferritinophagic Flux Was a Driving Force in Determination of Status of EMT, Ferroptosis, and NDRG1 Activation in Action of Mechanism of 2-Pyridylhydrazone Dithiocarbamate S-Acetic Acid.
Article in Journal of oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- NCOA4-mediated ferroptosis conducive to EMT inhibition in colorectal cancer cells was achieved through the PI3K/AKT/mTOR pathway.Scientific reports · 2025Article
- Ferritinophagy induced ferroptosis in the management of cancer.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- The induction of ferroptosis by KLF11/NCOA4 axis: the inhibitory role in clear cell renal cell carcinoma.Human cell · 2023Article
- Article
- Ferroptosis in Cancer Progression.Cells · 2023Review
- Role of Ferroptosis in Regulating the Epithelial-Mesenchymal Transition in Pulmonary Fibrosis.Biomedicines · 2023Review
- Prognostic prediction and immune infiltration analysis based on ferroptosis and EMT state in hepatocellular carcinoma.Frontiers in immunology · 2022Article
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Authors and funding
8 authors.
Funding
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Abstract
Ferritinophagy is a process of ferritin degradation in lysosomes; however, how its effect on other cellular events, such as epithelial-mesenchymal transition (EMT) and ferroptosis remains elusive. In this study, we determined how ferritinophagic flux influence the status of EMT and ferroptosis in HepG2 cell. Our data revealed that 2-pyridylhydrazone dithiocarbamate s-acetic acid (PdtaA) induced EMT inhibition involved ferritinophagy-mediated ROS production, but addition of ferrostatin-1 could attenuate the effect of PdtaA on the regulation of EMT-related proteins, suggesting that ferroptosis might involve in the EMT regulation. Next, downregulation of Gpx4 and xCT as well as enhanced lipid peroxidation further supported that PdtaA was able to induce ferroptosis. Knockdown of NCOA4 significantly attenuated the regulatory effect of PdtaA on related proteins which highlighted that the strength of ferritinophagic flux (NCOA4/ferritin) was a driving force in determination of the status of EMT and ferroptosis. Furthermore, NDRG1 activation was also observed, and knockdown of NDRG1 similarly influenced the expressions of ferroptosis-related proteins, suggesting that NDRG1 also involved ferroptosis induction, which was first reported. Taken together, PdtaA-induced EMT inhibition, ferroptosis, and NDRG1 activation all depended on the strength of ferritinophagic flux.
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Registered trials
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