Compound K [C-K; 20-O-(β-d-glucopyranosyl)-20(S)-protopanaxadiol], as a metabolite of ginsenoside, has been verified to have antitumor effects in various cancers, including non-small cell lung cancer (NSCLC). However, the detailed mechanisms of C-K in NSCLC remain
largely unknown. In this study, we aimed to evaluate the effect of C-K on apoptosis and autophagy in NSCLC cells as well as its related mechanisms. According to the results, C-K suppressed the proliferation, and led to G1 phase arrest and apoptosis in A549 and H1975 cells. Subsequently, C-K
promoted autophagy, as confirmed by the enhanced rate of cells staining positive with acridine orange, increased levels of LC3II and Beclin-1, and with decreased levels of p62 in A549 and H1975 cells. Moreover, 3-methyladenine (3-MA; an inhibitor of autophagy) effectively suppressed the inhibition
of proliferation and apoptosis that was induced with C-K. Finally, C-K treatment promoted the activation of the AMPK–mTOR and c-Jun N-terminal kinase (JNK) signaling pathways. Treatment with compound C (AMPK inhibitor) or SP600125 (JNK inhibitor) significantly restrained the inhibition
of proliferation, apoptosis, and autophagy induced with C-K in A549 and H1975 cells. In conclusion, this study demonstrates that C-K promotes autophagy-mediated apoptosis in NSCLC via AMPK–mTOR and JNK signaling pathways.
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cancer pulmonaire non à petites cellules;
non-small cell lung cancer
Document Type: Research Article
Department of Respiratory and Critical Care Medicine, Changhai Hospital, The Second Military Medical University, Shanghai 200433, People’s Republic of China.
Department of Gastroenterology, The First Hospital of Jilin University, Changchun 130021, People’s Republic of China.
Department of Respiratory Medicine, The General Hospital of First Automotive Works, The Fourth Hospital of Jilin University, Changchun 130011, People’s Republic of China.
Publication date: January 1, 2019
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