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Effects of ginkgol C17:1 on cisplatin-induced autophagy and apoptosis in HepG2 cells
Previous studies have demonstrated that ginkgol C17:1 significantly inhibits human liver cancer cells and enhances the anticancer activity of cisplatin in vivo and in vitro. However, the mechanism and biological function of ginkgol C17:1 on cells undergoing chemotherapy remain unclear. The aim of th...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5772831/ https://www.ncbi.nlm.nih.gov/pubmed/29399162 http://dx.doi.org/10.3892/ol.2017.7398 |
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author | Liu, Jun Li, Yueying Yang, Xiaoming Dong, Yan Wu, Jing Chen, Min |
author_facet | Liu, Jun Li, Yueying Yang, Xiaoming Dong, Yan Wu, Jing Chen, Min |
author_sort | Liu, Jun |
collection | PubMed |
description | Previous studies have demonstrated that ginkgol C17:1 significantly inhibits human liver cancer cells and enhances the anticancer activity of cisplatin in vivo and in vitro. However, the mechanism and biological function of ginkgol C17:1 on cells undergoing chemotherapy remain unclear. The aim of the present study was to determine the antitumor activity and mechanism of ginkgol C17:1 in combination with cisplatin in human hepatoblastoma HepG2 cells. The green fluorescent protein (GFP)-light chain 3 (LC3) adenovirus was transfected into HepG2 cells and autophagic flux was determined using fluorescence microscopy. Western blot analysis was also conducted to measure the expression of proteins associated with apoptosis, autophagy and their associated signaling pathways. Compared with the control group, autophagic flux and nucleus aberration rates were significantly increased (P<0.05), and the expression of proteins associated with autophagy and apoptosis were increased in the groups treated with cisplatin or ginkgol C17:1, respectively. However, following co-treatment with ginkgol C17:1 and cisplatin, the autophagic flux and the expression of autophagy proteins decreased; however, the nucleus aberration rate and apoptosis protein expression significantly increased (P<0.05) compared with the group treated with cisplatin alone. Additionally, the signaling pathways of autophagy and apoptosis were also activated following treatment with cisplatin, alone and in combination with ginkgol C17:1. Taken together, these results indicate that ginkgol C17:1 inhibits cisplatin-induced autophagy via AMP-activated protein kinase/ULK1signaling and increases cisplatin-induced apoptosis in HepG2 cells via the phosphoinositide 3-kinase/Akt/mechanistic target of rapamycin pathway. |
format | Online Article Text |
id | pubmed-5772831 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-57728312018-02-02 Effects of ginkgol C17:1 on cisplatin-induced autophagy and apoptosis in HepG2 cells Liu, Jun Li, Yueying Yang, Xiaoming Dong, Yan Wu, Jing Chen, Min Oncol Lett Articles Previous studies have demonstrated that ginkgol C17:1 significantly inhibits human liver cancer cells and enhances the anticancer activity of cisplatin in vivo and in vitro. However, the mechanism and biological function of ginkgol C17:1 on cells undergoing chemotherapy remain unclear. The aim of the present study was to determine the antitumor activity and mechanism of ginkgol C17:1 in combination with cisplatin in human hepatoblastoma HepG2 cells. The green fluorescent protein (GFP)-light chain 3 (LC3) adenovirus was transfected into HepG2 cells and autophagic flux was determined using fluorescence microscopy. Western blot analysis was also conducted to measure the expression of proteins associated with apoptosis, autophagy and their associated signaling pathways. Compared with the control group, autophagic flux and nucleus aberration rates were significantly increased (P<0.05), and the expression of proteins associated with autophagy and apoptosis were increased in the groups treated with cisplatin or ginkgol C17:1, respectively. However, following co-treatment with ginkgol C17:1 and cisplatin, the autophagic flux and the expression of autophagy proteins decreased; however, the nucleus aberration rate and apoptosis protein expression significantly increased (P<0.05) compared with the group treated with cisplatin alone. Additionally, the signaling pathways of autophagy and apoptosis were also activated following treatment with cisplatin, alone and in combination with ginkgol C17:1. Taken together, these results indicate that ginkgol C17:1 inhibits cisplatin-induced autophagy via AMP-activated protein kinase/ULK1signaling and increases cisplatin-induced apoptosis in HepG2 cells via the phosphoinositide 3-kinase/Akt/mechanistic target of rapamycin pathway. D.A. Spandidos 2018-01 2017-11-14 /pmc/articles/PMC5772831/ /pubmed/29399162 http://dx.doi.org/10.3892/ol.2017.7398 Text en Copyright: © Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Liu, Jun Li, Yueying Yang, Xiaoming Dong, Yan Wu, Jing Chen, Min Effects of ginkgol C17:1 on cisplatin-induced autophagy and apoptosis in HepG2 cells |
title | Effects of ginkgol C17:1 on cisplatin-induced autophagy and apoptosis in HepG2 cells |
title_full | Effects of ginkgol C17:1 on cisplatin-induced autophagy and apoptosis in HepG2 cells |
title_fullStr | Effects of ginkgol C17:1 on cisplatin-induced autophagy and apoptosis in HepG2 cells |
title_full_unstemmed | Effects of ginkgol C17:1 on cisplatin-induced autophagy and apoptosis in HepG2 cells |
title_short | Effects of ginkgol C17:1 on cisplatin-induced autophagy and apoptosis in HepG2 cells |
title_sort | effects of ginkgol c17:1 on cisplatin-induced autophagy and apoptosis in hepg2 cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5772831/ https://www.ncbi.nlm.nih.gov/pubmed/29399162 http://dx.doi.org/10.3892/ol.2017.7398 |
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