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Derrone induces autophagic cell death through induction of ROS and ERK in A549 cells

Identifieur interne : 000895 ( Main/Exploration ); précédent : 000894; suivant : 000896

Derrone induces autophagic cell death through induction of ROS and ERK in A549 cells

Auteurs : Myung-Ji Kang [Corée du Sud] ; Soo-Yeon Kim [Corée du Sud] ; Eun-Bin Kwon [Corée du Sud] ; Yang Hee Jo [Corée du Sud] ; Mi Kyeong Lee [Corée du Sud] ; Hyun-Sun Lee [Corée du Sud] ; Dong-Oh Moon [Corée du Sud] ; Mun-Ock Kim [Corée du Sud]

Source :

RBID : PMC:6583947

Abstract

We studied the effect of derrone (DR), one of the major compounds of unripe fruits of Cudrania tricuspidata, on cancer cell death. DR inhibited cell growth of various cancer cells, and that was partially associated with apoptosis in A549 cells. DR showed the autophagic features, such as the conversion of LC3-I to LC3-II, the formation of autophagosome and the downregulation of SQSTM1/p62 (p62). The treatment of autophagy inhibitor reversed DR-mediated cell death, suggesting that DR induces autophagic cell death. The increase of cytoplasmic Ca2+ and ROS by DR treatment significantly influences the formation of autophagosomes; however, only ROS scavengers significantly rescued the reduced cell viability. Additional results revealed that treatment of DR induces sustained phosphorylation of ERK and the inhibition of ERK phosphorylation using U0126 (ERK inhibitor) markedly attenuated DR-induced cell death. Overall, these results suggest that DR induces autophagic cell death through intracellular ROS and sustained ERK phosphorylation in A549 cells.


Url:
DOI: 10.1371/journal.pone.0218659
PubMed: 31216334
PubMed Central: 6583947


Affiliations:


Links toward previous steps (curation, corpus...)


Le document en format XML

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<p>We studied the effect of derrone (DR), one of the major compounds of unripe fruits of
<italic>Cudrania tricuspidata</italic>
, on cancer cell death. DR inhibited cell growth of various cancer cells, and that was partially associated with apoptosis in A549 cells. DR showed the autophagic features, such as the conversion of LC3-I to LC3-II, the formation of autophagosome and the downregulation of SQSTM1/p62 (p62). The treatment of autophagy inhibitor reversed DR-mediated cell death, suggesting that DR induces autophagic cell death. The increase of cytoplasmic Ca
<sup>2+</sup>
and ROS by DR treatment significantly influences the formation of autophagosomes; however, only ROS scavengers significantly rescued the reduced cell viability. Additional results revealed that treatment of DR induces sustained phosphorylation of ERK and the inhibition of ERK phosphorylation using U0126 (ERK inhibitor) markedly attenuated DR-induced cell death. Overall, these results suggest that DR induces autophagic cell death through intracellular ROS and sustained ERK phosphorylation in A549 cells.</p>
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</TEI>
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</affiliations>
</record>

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