IOCAS-IR  > 实验海洋生物学重点实验室
H1, a derivative of tetrandrine, enhances the efficacy of 5-FU in Bel7402/5-FU cells via suppressing STAT3/MCL-1 and inducing PUMA
Li, Fengli1; Wang, Jing2; Wu, Ning3,4; Zhang, Hua5; Li, Zheng1; Wei, Ning6,7
2019-11-26
Source PublicationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ISSN0006-291X
Volume520Issue:1Pages:93-98
Corresponding AuthorWang, Jing(wangjing2006050@126.com) ; Wei, Ning(chinaweining@yahoo.com)
AbstractCurrently, 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.
Keyword5-FU Drug resistance STAT3 Hepatocellular carcinoma MCL-1 PUMA
DOI10.1016/j.bbrc.2019.09.082
Indexed BySCI
Language英语
Funding ProjectChina National Natural Sciences Foundation[81202556]
WOS Research AreaBiochemistry & Molecular Biology ; Biophysics
WOS SubjectBiochemistry & Molecular Biology ; Biophysics
WOS IDWOS:000506410000015
PublisherACADEMIC PRESS INC ELSEVIER SCIENCE
Citation statistics
Cited Times:1[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.qdio.ac.cn/handle/337002/164173
Collection实验海洋生物学重点实验室
Corresponding AuthorWang, Jing; Wei, Ning
Affiliation1.Tianjin Univ Tradit Chinese Med, Teaching Hosp 1, Tianjin, Peoples R China
2.Jinzhou Med Univ, Affiliated Hosp 1, Jinzhou, Peoples R China
3.Chinese Acad Sci, Inst Oceanol, Key Lab Expt Marine Biol, Qingdao, Peoples R China
4.Qingdao Natl Lab Marine Sci & Technol, Lab Marine Drugs & Bioprod, Qingdao, Peoples R China
5.Jinzhou Med Univ, Jinzhou, Peoples R China
6.Univ Pittsburgh, Sch Med, Dept Med, Div Hematol Oncol, Pittsburgh, PA 15232 USA
7.Univ Pittsburgh, UPMC Hillman Canc Ctr, Canc Therapeut Program, Pittsburgh, PA 15232 USA
Recommended Citation
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.
Files in This Item:
There are no files associated with this item.
Related Services
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Google Scholar
Similar articles in Google Scholar
[Li, Fengli]'s Articles
[Wang, Jing]'s Articles
[Wu, Ning]'s Articles
Baidu academic
Similar articles in Baidu academic
[Li, Fengli]'s Articles
[Wang, Jing]'s Articles
[Wu, Ning]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[Li, Fengli]'s Articles
[Wang, Jing]'s Articles
[Wu, Ning]'s Articles
Terms of Use
No data!
Social Bookmark/Share
All comments (0)
No comment.
 

Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.