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Zn(-pr-thiosal) 配合物通过诱导细胞凋亡和 G1/S 细胞周期阻滞来抑制小鼠乳腺癌生长。

The Zn(-pr-thiosal) complex attenuates murine breast cancer growth by inducing apoptosis and G1/S cell cycle arrest.

机构信息

Department of Transfusiology, Pula General Hospital, Pula, 52100, Croatia.

Department of Cytology, Pula General Hospital, Pula, 52100, Croatia.

出版信息

Future Med Chem. 2020 May;12(10):897-914. doi: 10.4155/fmc-2019-0215. Epub 2020 Apr 8.

DOI:10.4155/fmc-2019-0215
PMID:32267176
Abstract

We investigated the antitumor effects of zinc(II) complex with -propyl thiosalicylic acid [Zn(-pr-thiosal)] in 4T1 murine breast cancer model.  The Zn(-pr-thiosal) complex reduced primary tumor growth and induced tumor cell apoptosis. The Zn(-pr-thiosal) complex disrupted the balance between pro- and antiapoptotic Bcl-2 family members in 4T1 cells and induced G1/S cell cycle arrest. The Zn(-pr-thiosal) complex increased the percentage of p16, p21 and p27 positive 4T1 cells. There was a significantly decrease in expression of STAT3 and its targets c-Myc and cyclin D3 in 4T1 cells treated with the Zn(-pr-thiosal) complex thus contributing to G1/S cell cycle arrest and/or apoptosis. Our data suggest that the Zn(-pr-thiosal) complex restricted tumor growth through induction of mitochondrial-driven apoptosis and suppression of cell cycle progression.

摘要

我们研究了 - 丙基硫代水杨酸锌（Zn(-pr-thiosal)）配合物在 4T1 小鼠乳腺癌模型中的抗肿瘤作用。该配合物降低了原发性肿瘤的生长，并诱导肿瘤细胞凋亡。Zn(-pr-thiosal)配合物破坏了 4T1 细胞中促凋亡和抗凋亡 Bcl-2 家族成员之间的平衡，并诱导 G1/S 细胞周期停滞。Zn(-pr-thiosal)配合物增加了 p16、p21 和 p27 阳性 4T1 细胞的百分比。Zn(-pr-thiosal)配合物处理的 4T1 细胞中 STAT3 及其靶标 c-Myc 和细胞周期蛋白 D3 的表达显著下降，从而导致 G1/S 细胞周期停滞和/或细胞凋亡。我们的数据表明，Zn(-pr-thiosal)配合物通过诱导线粒体驱动的细胞凋亡和抑制细胞周期进程来限制肿瘤生长。

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