RETRACTED: Trastuzumab-modified DM1-loaded nanoparticles for HER2+ breast cancer treatment: an in vitro and in vivo study (Retracted Article)

被引:15
作者
Rong, Ling [1 ,2 ]
Zhou, Shuping [3 ,4 ]
Liu, Xinkuang [3 ,4 ]
Li, Amin [3 ,4 ]
Jing, Tao [2 ]
Liu, Xueke [2 ]
Zhang, Yinci [2 ]
Cai, Shiyu [2 ]
Tang, Xiaolong [1 ,2 ]
机构
[1] Anhui Univ Sci & Technol, Bozhou Peoples Hosp, Med Coll, Bozhou, Peoples R China
[2] Anhui Univ Sci & Technol, Med Coll, Huainan, Peoples R China
[3] Anhui Univ Sci & Technol, Huainan Peoples Hosp 1, Huainan, Peoples R China
[4] Anhui Univ Sci & Technol, Affiliated Hosp 1, Med Coll, Huainan, Peoples R China
关键词
Emtansine (DM1); targeting nanoparticles; drug delivery; HER2(+) tumors; GROWTH-FACTOR RECEPTOR; SRC; LAPATINIB; EMTANSINE; CELLS; TPGS; CAPECITABINE; RESISTANCE; INHIBITION; EXPRESSION;
D O I
10.1080/21691401.2017.1391821
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Background: Emtansine (DM1) is a highly potent anti-microtubule agent that has shown promising results for breast cancer treatment, but side effects limit its widespread clinical use. In this research, a new nano-drug was developed to integrate DM1 agent with antibody targeting. Methods: A system of novel nanoparticles (NPs) DM1-NPs-trastuzumab (DM1-NPs-Tmab) of DM1 combined with (anti-HER2 antibody, Herceptin (R), Trastuzumab) was developed for HER2(+) breast cancer treatment, and its physical characterization and antitumor biological activity were investigated. Results: DM1-NPs-Tmab-targeted HER2(+) breast cancer cells specifically were developed. Compared with naked DM1 and Herceptin, DM1-NPs-Tmab showed greater toxicity on HER2(+) cancer cells and blocked the HER2-PI3K/Akt cell activation pathway. DM1-NPs-Tmab inhibited tumor growth by 88% and had less toxic effects in vivo than non-targeting DM1 when administered to MDA-MB-453 xenograft bearing mice. Conclusion: DM1-NPs-Tmab shows superior anti-tumor efficacy than free Herceptin or DM1. DM1-NPs-Tmab is a potential promising formulation for targeting biotherapy of HER2(+) tumors.
引用
收藏
页码:1708 / 1718
页数:11
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