H1, a derivative of tetrandrine, enhances the efficacy of 5-FU in Bel7402/5-FU cells via suppressing STAT3/MCL-1 and inducing PUMA
文献类型:期刊论文
作者 | Li, Fengli7; Wang, Jing6; Wu, Ning1,5; Zhang, Hua4; Li, Zheng7; Wei, Ning2,3 |
刊名 | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
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出版日期 | 2019-11-26 |
卷号 | 520期号:1页码:93-98 |
关键词 | 5-FU Drug resistance STAT3 Hepatocellular carcinoma MCL-1 PUMA |
ISSN号 | 0006-291X |
DOI | 10.1016/j.bbrc.2019.09.082 |
通讯作者 | Wang, Jing(wangjing2006050@126.com) ; Wei, Ning(chinaweining@yahoo.com) |
英文摘要 | Currently, 5-fluorouracil (5-FU) resistance became a major obstacle to its clinical use for patients with hepatocellular carcinoma (HCC). It's urgent to develop a novel strategy for enhancing the therapeutic efficacy of 5-FU. Herein, we found that H1 (a derivative of Tetrandrine) exerted a potent anti-MDR effect on growth of 5-FU resistant HCC cells (Be17402/5FU). The resistant fold (RF) of 5-FU is over 160-fold, while the RF of H1 is only 4.8-fold in Be17402/5-FU cells. Further studies demonstrated that blockage of STAT3/MCL-1 signaling and induction of PUMA is responsible to anti-MDR activity of H1. Moreover, combination of H1 and 5-FU (Ratio = 1:2) could synergistically induce apoptosis of Be17402/5-FU cells. Co-treatment of H1 enhances the suppression of p-STAT3 and MCL-1, and significantly increases PUMA expression. Finally, the combination of H1 and 5-FU results in an increase of cleaved PARP. Taken together, H1 effectively improve the cytotoxic effect of 5-FU against Be17402/5-FU cells via blocking STAT3/MCL-1 pathway and inducing PUMA. Our findings suggested that combination 5-FU with anti-MDR agents might present a novel strategy to enhance the therapeutic efficacy of 5-FU in resistant HCC. (C) 2019 Elsevier Inc. All rights reserved. |
资助项目 | China National Natural Sciences Foundation[81202556] |
WOS研究方向 | Biochemistry & Molecular Biology ; Biophysics |
语种 | 英语 |
WOS记录号 | WOS:000506410000015 |
出版者 | ACADEMIC PRESS INC ELSEVIER SCIENCE |
源URL | [http://ir.qdio.ac.cn/handle/337002/164172] ![]() |
专题 | 海洋研究所_实验海洋生物学重点实验室 |
通讯作者 | Wang, Jing; Wei, Ning |
作者单位 | 1.Qingdao Natl Lab Marine Sci & Technol, Lab Marine Drugs & Bioprod, Qingdao, Peoples R China 2.Univ Pittsburgh, UPMC Hillman Canc Ctr, Canc Therapeut Program, Pittsburgh, PA 15232 USA 3.Univ Pittsburgh, Sch Med, Dept Med, Div Hematol Oncol, Pittsburgh, PA 15232 USA 4.Jinzhou Med Univ, Jinzhou, Peoples R China 5.Chinese Acad Sci, Inst Oceanol, Key Lab Expt Marine Biol, Qingdao, Peoples R China 6.Jinzhou Med Univ, Affiliated Hosp 1, Jinzhou, Peoples R China 7.Tianjin Univ Tradit Chinese Med, Teaching Hosp 1, Tianjin, Peoples R China |
推荐引用方式 GB/T 7714 | Li, Fengli,Wang, Jing,Wu, Ning,et al. H1, a derivative of tetrandrine, enhances the efficacy of 5-FU in Bel7402/5-FU cells via suppressing STAT3/MCL-1 and inducing PUMA[J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,2019,520(1):93-98. |
APA | Li, Fengli,Wang, Jing,Wu, Ning,Zhang, Hua,Li, Zheng,&Wei, Ning.(2019).H1, a derivative of tetrandrine, enhances the efficacy of 5-FU in Bel7402/5-FU cells via suppressing STAT3/MCL-1 and inducing PUMA.BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,520(1),93-98. |
MLA | Li, Fengli,et al."H1, a derivative of tetrandrine, enhances the efficacy of 5-FU in Bel7402/5-FU cells via suppressing STAT3/MCL-1 and inducing PUMA".BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 520.1(2019):93-98. |
入库方式: OAI收割
来源:海洋研究所
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