Zheng Yuzhu, Zhao Ying-Lan, Deng Xiaoqiang, Yang Shengyong, Mao Yongqiu, Li Zhengguang, Jiang Peidu, Zhao Xia, Wei Yuquan
State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University, Chengdu, China.
Cancer Invest. 2009 Mar;27(3):286-92. doi: 10.1080/07357900802427927.
The present study was to investigate the anticancer effect of chloroquine on proliferation of mouse colon cancer cell line CT26 in vivo and in vitro and the possible mechanism. We found that chloroquine inhibited CT26 proliferation by concentration- and time-dependent manner. This effect was associated with apoptosis induction and decreased level of phosphorylated p42/44 mitogen-activated protein kinase and phosphorylated Akt. The in vivo study showed chloroquine-reduced tumor volume and prolonged survival time in CT26-bearing mice. These observations indicated chloroquine could inhibit CT26 proliferation by inducing apoptosis both in vitro and in vivo, providing its chemotherapeutic potential of human cancers.
本研究旨在探讨氯喹对小鼠结肠癌细胞系CT26体内外增殖的抗癌作用及其可能机制。我们发现氯喹以浓度和时间依赖性方式抑制CT26增殖。这种作用与诱导凋亡以及磷酸化的p42/44丝裂原活化蛋白激酶和磷酸化的Akt水平降低有关。体内研究表明氯喹可减小荷CT26小鼠的肿瘤体积并延长其生存时间。这些观察结果表明氯喹可通过在体外和体内诱导凋亡来抑制CT26增殖,提示其对人类癌症的化疗潜力。