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Combining use of Phillyrin and autophagy blocker alleviates laryngeal squamous cell carcinoma via AMPK/mTOR/p70S6K signaling

Identifieur interne : 000942 ( Main/Exploration ); précédent : 000941; suivant : 000943

Combining use of Phillyrin and autophagy blocker alleviates laryngeal squamous cell carcinoma via AMPK/mTOR/p70S6K signaling

Auteurs : Da-Hua Wang [République populaire de Chine] ; Xi He [République populaire de Chine] ; Qing He [République populaire de Chine]

Source :

RBID : PMC:6616054

Abstract

Phillyrin (PHN), one of the major active constituents of Forsythia suspensa and F. koreana, has been reported to produce antioxidant, antibacterial, anti-obesity and anti-inflammatory effects. However, no study has demonstrated the role of PHN in laryngeal squamous cell carcinoma (LSCC). We aimed to investigate the effects of PHN on the proliferation and apoptosis of HEp-2 cells. In the present study, PHN alone showed little effect on HEp-2 cell proliferation and apoptosis. Subsequent tests showed that PHN could largely enhance the level of autophagy on HEp-2 cells. Combining use of PHN and autophagy blockers including 3-methyladenine (3-MA) and chloroquine (CQ) significantly inhibited HEp-2 cell proliferation in a dose- and time-dependent manner and induced apoptosis after 24 h in a dose-dependent manner. Additionally, we found that the possible underlying molecular mechanism of PHN-induced autophagy might be through the AMPK/mTOR/p70S6K signaling pathway. Taken together, our study indicates that combining use of PHN and autophagy blockers may serve as a novel strategy in LSCC treatment.


Url:
DOI: 10.1042/BSR20190459
PubMed: 31147451
PubMed Central: 6616054


Affiliations:


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


Le document en format XML

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<p>Phillyrin (PHN), one of the major active constituents of
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<name sortKey="He, Qing" sort="He, Qing" uniqKey="He Q" first="Qing" last="He">Qing He</name>
<name sortKey="He, Xi" sort="He, Xi" uniqKey="He X" first="Xi" last="He">Xi He</name>
</country>
</tree>
</affiliations>
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