Ferritinophagic Flux Activation in CT26 Cells Contributed to EMT Inhibition Induced by a Novel Iron Chelator, DpdtpA
Identifieur interne : 000817 ( Main/Exploration ); précédent : 000816; suivant : 000818Ferritinophagic Flux Activation in CT26 Cells Contributed to EMT Inhibition Induced by a Novel Iron Chelator, DpdtpA
Auteurs : Yanjie Sun [République populaire de Chine] ; Cuiping Li [République populaire de Chine] ; Jiankang Feng [République populaire de Chine] ; Yongli Li [République populaire de Chine] ; Xinbo Zhai [République populaire de Chine] ; Lei Zhang [République populaire de Chine] ; Changzheng Li [République populaire de Chine]Source :
- Oxidative Medicine and Cellular Longevity [ 1942-0900 ] ; 2019.
Abstract
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
Url:
DOI: 10.1155/2019/8753413
PubMed: 31320987
PubMed Central: 6610730
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>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 (IC<sub>50</sub>
= 1.5 ± 0.2 <italic>μ</italic>
M), 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-<italic>β</italic>
1 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.</p>
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<affiliations><list><country><li>République populaire de Chine</li>
</country>
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<tree><country name="République populaire de Chine"><noRegion><name sortKey="Sun, Yanjie" sort="Sun, Yanjie" uniqKey="Sun Y" first="Yanjie" last="Sun">Yanjie Sun</name>
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<name sortKey="Li, Changzheng" sort="Li, Changzheng" uniqKey="Li C" first="Changzheng" last="Li">Changzheng Li</name>
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</record>
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