Anti-tumor activity and the mechanism of a green tea (Camellia sinensis) polysaccharide on prostate cancer

被引:37
|
作者
Yang, Ke [1 ]
Gao, Zhi-Yong [1 ]
Li, Tie-Qiu [1 ]
Song, Wei [1 ]
Xiao, Wei [1 ]
Zheng, Jue [1 ]
Chen, Hao [1 ]
Chen, Gui-Heng [1 ]
Zou, Hao-Yu [2 ]
机构
[1] Hunan Normal Univ, Affiliated Hosp 1, Hunan Prov Peoples Hosp, Dept Urol, Changsha 410005, Hunan, Peoples R China
[2] Hunan Normal Univ, Affiliated Hosp 1, Hunan Prov Peoples Hosp, Dept Surg, Changsha 410005, Hunan, Peoples R China
关键词
Green tea polysaccharide; Prostate cancer; MicroRNA-93; CELL-GROWTH; MICRORNA; EXPRESSION; PROLIFERATION; PURIFICATION; PROGRESSION; EXTRACTION; APOPTOSIS; INVASION; MEN;
D O I
10.1016/j.ijbiomac.2018.10.101
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
In this study, a homogeneous polysaccharide (GTP), with a molecular weight of 7.0 x 10(4) Da, was isolated from Green tea, which was only composed of glucose. The antitumor effects of GTP on prostate cancer (PC) cell line along with the possible mechanism was examined. First, we investigate the potential role of microRNA-93 (miR-93) in PC progression. Our results showed that miR-93 was significantly upregulated in human PC tissues and several PC cell lines, and its overexpression was correlated with poor survival in PC patients. Furthermore, functional analysis showed that miR-93 overexpression promoted the migration, invasion and proliferation of PC-3 cells transfected with miR-93 mimics, while its knockdown displayed an opposite result in DU145 cells following miR-93 inhibitor transfection. Additionally, in vivo tumorigenic studies on nude mice confirmed that miR93 mimic treatment accelerated the growth of PC-3 xenograft tumors. As expected, GTP (25, 50 and 100 mu g/ml) inhibited growth of PC-3 cells via inducing apoptosis, which was achieved by elevation of bax/bcl-2 ratio and caspae-3 protein expression, as well as a decrease of miR-93. Thus, miR-93 may be a potential therapeutic target by GTP for PC therapy. (C) 2018 Elsevier B.V. All rights reserved.
引用
收藏
页码:95 / 103
页数:9
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