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Ferritinophagic Flux Activation in CT26 Cells Contributed to EMT Inhibition Induced by a Novel Iron Chelator, DpdtpA
Joint Authors
Li, Changzheng
Li, Yongli
Sun, Yanjie
Li, Cuiping
Feng, Jiankang
Zhai, Xinbo
Zhang, Lei
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-14, 14 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-06-20
Country of Publication
Egypt
No. of Pages
14
Main Subjects
Abstract EN
Epithelial-mesenchymal transition (EMT) contributes to metastasis and drug resistance; inhibition of EMT may attenuate metastasis and drug resistance.
It has been demonstrated that ferritinophagy involves the process of many diseases; however, the relationship between EMT and ferritinophagy was not fully established.
Some iron chelators show the ability to inhibit EMT, but whether ferritinophagy plays a role in EMT is largely unknown.
To this end, we investigated the effect of a novel iron chelator, DpdtpA (2,2 ′-di-pyridylketone dithiocarbamate propionic acid), on EMT in the CT26 cell line.
The DpdtpA displayed excellent antitumor (IC50=1.5±0.2 μM), leading to ROS production and apoptosis occurrence.
Moreover, the ROS production correlated with ferritin degradation.
The upregulation of LC3-II and NCOA4 from immunofluorescence and Western blotting analysis revealed that the occurrence of ferritinophagy contributed to ROS production.
Furthermore, DpdtpA could induce an alteration both in morphology and in epithelial-mesenchymal markers, displaying significant EMT inhibition.
The correlation analysis revealed that DpdtpA-induced ferritinophagy contributed to the EMT inhibition, implying that NCOA4 involved EMT process, which was firstly reported.
To reinforce this concept, the ferritinophagic flux (NCOA4/ferritin) in either treated by TGF-β1 or combined with DpdtpA was determined.
The results indicated that activating ferritinophagic flux would enhance ROS production which accordingly suppressed EMT or implementing the EMT suppression seemed to be through “fighting fire with fire” strategy.
Taken together, our data demonstrated that ferritinophagic flux was a dominating driving force in EMT proceeding, and the new finding definitely will enrich our knowledge of ferritinophagy in EMT process.
American Psychological Association (APA)
Sun, Yanjie& Li, Cuiping& Feng, Jiankang& Li, Yongli& Zhai, Xinbo& Zhang, Lei…[et al.]. 2019. Ferritinophagic Flux Activation in CT26 Cells Contributed to EMT Inhibition Induced by a Novel Iron Chelator, DpdtpA. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-14.
https://search.emarefa.net/detail/BIM-1205912
Modern Language Association (MLA)
Sun, Yanjie…[et al.]. Ferritinophagic Flux Activation in CT26 Cells Contributed to EMT Inhibition Induced by a Novel Iron Chelator, DpdtpA. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-14.
https://search.emarefa.net/detail/BIM-1205912
American Medical Association (AMA)
Sun, Yanjie& Li, Cuiping& Feng, Jiankang& Li, Yongli& Zhai, Xinbo& Zhang, Lei…[et al.]. Ferritinophagic Flux Activation in CT26 Cells Contributed to EMT Inhibition Induced by a Novel Iron Chelator, DpdtpA. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-14.
https://search.emarefa.net/detail/BIM-1205912
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1205912