Chitosan-coated doxorubicin nano-particles drug delivery system inhibits cell growth of liver cancer via p53/PRC1 pathway

被引:53
作者
Ye, Bai-liang [1 ]
Zheng, Ru [1 ]
Ruan, Xiao-jiao [1 ]
Zheng, Zhi-hai [1 ]
Cai, Hua-jie [1 ]
机构
[1] Wenzhou Med Univ, Affiliated Hosp 1, Dept Gen Surg, Nan Bai Xiang St, Wenzhou 325000, Zhejiang, Peoples R China
关键词
Chitosan; Doxorubicin; Nano-particles; FA-CS-DOX; p53; IN-VIVO; NANOPARTICLES; P53; CARCINOMA; THERAPY; TARGET; PRC1;
D O I
10.1016/j.bbrc.2017.10.156
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: Nano-particles have been widely used in target-specific drug delivery system and showed advantages in cancers treatment. This study aims to evaluate the effect of chitosan coated doxorubicin nano-particles drug delivery system in liver cancer. Methods: The chitosan nano-particles were prepared by using the ionic gelation method. The characterizations of the nano-particles were determined by transmission electron microscopy. The cytotoxicity was detected by WITT assay, and the endocytosis, cell apoptosis and cell cycle were examined by flow cytometry. The protein level was analyzed with western blot. The dual luciferase reporter assay was performed to assess the interaction between p53 and the promoter of PRC1, and chromatin immune precipitation was used to verify the binding between them. Results: The FA-CS-DOX nano-particles were irregular and spherical particles around 30-40 nm, with uniform size and no adhesion. No significant difference was noted in doxorubicin release rate between CS-DOX and FA-CS-DOX. FA-CS-DOX nano-particles showed stronger cytotoxicity than CS-DOX. FA-CSDOX nano-particles promoted the apoptosis and arrested cell cycle at G2/M phase, and they up-regulated p53. FA-CS-DOX nano-particles inhibited cell survival through p53/PRC1 pathway. Conclusion: Chitosan-coated doxorubicin nano-particles drug delivery system inhibits cell growth of liver cancer by promoting apoptosis and arresting cell cycle at G2/M phase through p53/PRC1 pathway. (C) 2017 Elsevier Inc. All rights reserved.
引用
收藏
页码:414 / 420
页数:7
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