摘要
原文 | 英語 |
---|---|
頁(從 - 到) | 3229-3234 |
頁數 | 6 |
期刊 | Oncology Letters |
卷 | 14 |
發行號 | 3 |
DOIs | |
出版狀態 | 已發佈 - 2017 |
指紋
ASJC Scopus subject areas
- Oncology
- Cancer Research
引用此文
Amentoflavone enhances sorafenib-induced apoptosis through extrinsic and intrinsic pathways in sorafenib-resistant hepatocellular carcinoma SK-hep1 cells in vitro. / Chen, Wei Lung; Hsieh, Chia Ling; Chen, Jiann Hwa; Huang, Chih Sheng; Chen, Wei Ting; Kuo, Yu Cheng; Chen, Cheng Yu; Hsu, Fei Ting.
於: Oncology Letters, 卷 14, 編號 3, 2017, p. 3229-3234.研究成果: 雜誌貢獻 › 文章
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TY - JOUR
T1 - Amentoflavone enhances sorafenib-induced apoptosis through extrinsic and intrinsic pathways in sorafenib-resistant hepatocellular carcinoma SK-hep1 cells in vitro
AU - Chen, Wei Lung
AU - Hsieh, Chia Ling
AU - Chen, Jiann Hwa
AU - Huang, Chih Sheng
AU - Chen, Wei Ting
AU - Kuo, Yu Cheng
AU - Chen, Cheng Yu
AU - Hsu, Fei Ting
PY - 2017
Y1 - 2017
N2 - The present study aimed to evaluate the effects of amentoflavone on sorafenib-induced apoptosis in sorafenib-resistant hepatocellular carcinoma (HCC) cells. The sorafenib-resistant SK-Hep1 (SK-Hep1R) cell line was established for the present study. Initially, the differences in sorafenib-induced cytotoxicity and apoptosis between wild-type SK-Hep1 and SK-Hep1R cells were verified using the MTT assay and flow cytometry. The effects of amentoflavone on sorafenib-induced cytotoxicity and apoptosis were then investigated using MTT, flow cytometry, DNA gel electrophoresis and western blot analysis. The results demonstrated that cell viability of SK-Hep1R cells was increased compared with that of SK-Hep1 cells following treatment with different concentrations of sorafenib for 24 h. Apoptosis of SK-Hep1R cells was lower than that of SK-Hep1 cells following treatment with 20 µM sorafenib for 24 h. Amentoflavone alone did not inhibit cell viability but significantly triggered sorafenib-induced cytotoxicity and apoptosis in SK-Hep1R cells. Amentoflavone not only reversed sorafenib-induced anti-apoptotic protein levels but also enhanced sorafenib-induced pro-apoptotic protein expression in SK-Hep1R cells. In conclusion, amentoflavone may be used as a sorafenib sensitizer to enhance sorafenib-induced cytotoxicity and trigger sorafenib-induced apoptosis through extrinsic and intrinsic pathways in SK-Hep1R cells.
AB - The present study aimed to evaluate the effects of amentoflavone on sorafenib-induced apoptosis in sorafenib-resistant hepatocellular carcinoma (HCC) cells. The sorafenib-resistant SK-Hep1 (SK-Hep1R) cell line was established for the present study. Initially, the differences in sorafenib-induced cytotoxicity and apoptosis between wild-type SK-Hep1 and SK-Hep1R cells were verified using the MTT assay and flow cytometry. The effects of amentoflavone on sorafenib-induced cytotoxicity and apoptosis were then investigated using MTT, flow cytometry, DNA gel electrophoresis and western blot analysis. The results demonstrated that cell viability of SK-Hep1R cells was increased compared with that of SK-Hep1 cells following treatment with different concentrations of sorafenib for 24 h. Apoptosis of SK-Hep1R cells was lower than that of SK-Hep1 cells following treatment with 20 µM sorafenib for 24 h. Amentoflavone alone did not inhibit cell viability but significantly triggered sorafenib-induced cytotoxicity and apoptosis in SK-Hep1R cells. Amentoflavone not only reversed sorafenib-induced anti-apoptotic protein levels but also enhanced sorafenib-induced pro-apoptotic protein expression in SK-Hep1R cells. In conclusion, amentoflavone may be used as a sorafenib sensitizer to enhance sorafenib-induced cytotoxicity and trigger sorafenib-induced apoptosis through extrinsic and intrinsic pathways in SK-Hep1R cells.
KW - Amentoflavone
KW - Apoptosis
KW - Hepatocellular carcinoma
KW - Resistance
KW - Sorafenib
UR - http://www.scopus.com/inward/record.url?scp=85026304683&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85026304683&partnerID=8YFLogxK
U2 - 10.3892/ol.2017.6540
DO - 10.3892/ol.2017.6540
M3 - Article
AN - SCOPUS:85026304683
VL - 14
SP - 3229
EP - 3234
JO - Oncology Letters
JF - Oncology Letters
SN - 1792-1074
IS - 3
ER -