Ecliptasaponin A induces apoptosis through the activation of ASK1/JNK pathway and autophagy in human lung cancer cells
Identifieur interne : 000861 ( Main/Exploration ); précédent : 000860; suivant : 000862Ecliptasaponin A induces apoptosis through the activation of ASK1/JNK pathway and autophagy in human lung cancer cells
Auteurs : Jia Han ; Wang Lv ; Hongxu Sheng ; Yiqing Wang ; Longxiang Cao ; Sha Huang ; Linhai Zhu ; Jian HuSource :
- Annals of Translational Medicine [ 2305-5839 ] ; 2019.
Abstract
Non-small cell lung cancer (NSCLC) is one of the causes of carcinomas mortality worldwide. Ecliptasaponin A (ES), a natural product extracted from the plant known as Eclipta prostrata, has been reported as an anti-cancer drug against various cancer cell lines. However, the exact mechanisms of ES have not yet been fully characterized.
Numerous studies have been done to support that ES has a powerful inhibiting effect on the growth of cancers via the activation of apoptosis and autophagy. To explore the underlying mechanisms of anti-cancer and investigate the relationships of the apoptosis and autophagy, we used apoptosis signal-regulating kinase 1 (ASK1) inhibitor (GS-4997), c-Jun N-terminal kinase (JNK) inhibitor (SP600125), and autophagy inhibitor [chloroquine (CQ) and 3-methyladenine (3-MA)].
ES could potently suppress cell viability and induces apoptotic cell death of human lung cancer cells H460 and H1975. ES activated apoptosis via ASK1/JNK pathway, GS-4997 and SP600125 can attenuated these effects. Furthermore, ES could triggered autophagy in lung cancer cell lines, and the autophagy inhibitor 3-MA and CQ reversed ES-induced apoptosis in H460 and H1975 cells. Furthermore, SP600125 can inhibit autophagy.
This study showed that ES induces apoptosis in human lung cancer cells by triggering enhanced autophagy and ASK1/JNK pathway, which may thus be a promising agent against lung cancer.
Url:
DOI: 10.21037/atm.2019.10.07
PubMed: 31807521
PubMed Central: 6861768
Affiliations:
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<author><name sortKey="Lv, Wang" sort="Lv, Wang" uniqKey="Lv W" first="Wang" last="Lv">Wang Lv</name>
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<author><name sortKey="Sheng, Hongxu" sort="Sheng, Hongxu" uniqKey="Sheng H" first="Hongxu" last="Sheng">Hongxu Sheng</name>
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<author><name sortKey="Lv, Wang" sort="Lv, Wang" uniqKey="Lv W" first="Wang" last="Lv">Wang Lv</name>
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<author><name sortKey="Sheng, Hongxu" sort="Sheng, Hongxu" uniqKey="Sheng H" first="Hongxu" last="Sheng">Hongxu Sheng</name>
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<author><name sortKey="Wang, Yiqing" sort="Wang, Yiqing" uniqKey="Wang Y" first="Yiqing" last="Wang">Yiqing Wang</name>
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<author><name sortKey="Cao, Longxiang" sort="Cao, Longxiang" uniqKey="Cao L" first="Longxiang" last="Cao">Longxiang Cao</name>
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<author><name sortKey="Huang, Sha" sort="Huang, Sha" uniqKey="Huang S" first="Sha" last="Huang">Sha Huang</name>
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<author><name sortKey="Zhu, Linhai" sort="Zhu, Linhai" uniqKey="Zhu L" first="Linhai" last="Zhu">Linhai Zhu</name>
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<author><name sortKey="Hu, Jian" sort="Hu, Jian" uniqKey="Hu J" first="Jian" last="Hu">Jian Hu</name>
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<series><title level="j">Annals of Translational Medicine</title>
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>Non-small cell lung cancer (NSCLC) is one of the causes of carcinomas mortality worldwide. Ecliptasaponin A (ES), a natural product extracted from the plant known as Eclipta prostrata, has been reported as an anti-cancer drug against various cancer cell lines. However, the exact mechanisms of ES have not yet been fully characterized.</p>
</sec>
<sec><title>Methods</title>
<p>Numerous studies have been done to support that ES has a powerful inhibiting effect on the growth of cancers via the activation of apoptosis and autophagy. To explore the underlying mechanisms of anti-cancer and investigate the relationships of the apoptosis and autophagy, we used apoptosis signal-regulating kinase 1 (ASK1) inhibitor (GS-4997), c-Jun N-terminal kinase (JNK) inhibitor (SP600125), and autophagy inhibitor [chloroquine (CQ) and 3-methyladenine (3-MA)].</p>
</sec>
<sec><title>Results</title>
<p>ES could potently suppress cell viability and induces apoptotic cell death of human lung cancer cells H460 and H1975. ES activated apoptosis via ASK1/JNK pathway, GS-4997 and SP600125 can attenuated these effects. Furthermore, ES could triggered autophagy in lung cancer cell lines, and the autophagy inhibitor 3-MA and CQ reversed ES-induced apoptosis in H460 and H1975 cells. Furthermore, SP600125 can inhibit autophagy.</p>
</sec>
<sec><title>Conclusions</title>
<p>This study showed that ES induces apoptosis in human lung cancer cells by triggering enhanced autophagy and ASK1/JNK pathway, which may thus be a promising agent against lung cancer.</p>
</sec>
</div>
</front>
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<name sortKey="Hu, Jian" sort="Hu, Jian" uniqKey="Hu J" first="Jian" last="Hu">Jian Hu</name>
<name sortKey="Huang, Sha" sort="Huang, Sha" uniqKey="Huang S" first="Sha" last="Huang">Sha Huang</name>
<name sortKey="Lv, Wang" sort="Lv, Wang" uniqKey="Lv W" first="Wang" last="Lv">Wang Lv</name>
<name sortKey="Sheng, Hongxu" sort="Sheng, Hongxu" uniqKey="Sheng H" first="Hongxu" last="Sheng">Hongxu Sheng</name>
<name sortKey="Wang, Yiqing" sort="Wang, Yiqing" uniqKey="Wang Y" first="Yiqing" last="Wang">Yiqing Wang</name>
<name sortKey="Zhu, Linhai" sort="Zhu, Linhai" uniqKey="Zhu L" first="Linhai" last="Zhu">Linhai Zhu</name>
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