Chen Xiaochao, Yang Xiangdong, Mu Jiefei, Yue Chaochi
Department of Anorectal, Chengdu Anorectal Hospital, Chengdu 610000, China.
Department of Anorectal, Dayi County Hospital of Traditional Chinese Medicine, Chengdu 610000, China.
Transl Cancer Res. 2020 May;9(5):3203-3213. doi: 10.21037/tcr-20-940.
Despite the advances in the diagnosis and treatment of colon cancer, the disease remains a major threat worldwide. Ligustrazine (LSZ) is an alkaloid with anti-tumor activity. This study aimed to elucidate the anti-tumor qualities of LSZ on colon cancer cells and , as well as its involved mechanism.
In this study, CCK-8, colony formation, transwell invasion assay and flow cytometry were employed to examined the cells behaviors. Moreover, the proteins related to the epithelial mesenchymal transformation (EMT) process were determined by RT-qPCR and western blotting. Then, the expression of PI3K, AKT, and mTOR were tested by western blotting. Furthermore, a xenograft mouse model was used to investigate the role of LSZ .
LSZ treatment (0.1, 0.5 and 1.5 mM) significantly inhibited SW480 cells' efforts to proliferate, migrate and invade and also induced SW480 cell apoptosis. In addition, LSZ inhibited EMT process. Meanwhile, Western blotting indicated that LSZ treatment administered on a dose-dependent basis inhibited the phosphorylation of PI3K, AKT, and mTOR. Furthermore, in our animal experiments, the weight of colon cancer was significantly lower in LSZ-treated mice than in untreated ones, and the expression of Ki67 and N-cadherin positive cells was significantly lower in the treated mice than in their control group counterparts.
Together, the results suggested that LSZ inhibited proliferation, motility, and EMT of colon cancer cells through the PI3K/AKT/mTOR pathway and .
尽管结肠癌的诊断和治疗取得了进展，但该疾病在全球范围内仍然是一个重大威胁。川芎嗪（LSZ）是一种具有抗肿瘤活性的生物碱。本研究旨在阐明LSZ对结肠癌细胞的抗肿瘤特性及其相关机制。
在本研究中，采用CCK-8、集落形成、Transwell侵袭试验和流式细胞术检测细胞行为。此外，通过RT-qPCR和蛋白质印迹法测定与上皮-间质转化（EMT）过程相关的蛋白质。然后，通过蛋白质印迹法检测PI3K、AKT和mTOR的表达。此外，还使用异种移植小鼠模型研究LSZ的作用。
LSZ处理（0.1、0.5和1.5 mM）显著抑制SW480细胞的增殖、迁移和侵袭，并诱导SW480细胞凋亡。此外，LSZ抑制EMT过程。同时，蛋白质印迹表明，LSZ处理以剂量依赖的方式抑制PI3K、AKT和mTOR的磷酸化。此外，在我们的动物实验中，LSZ处理的小鼠结肠癌重量显著低于未处理的小鼠，且处理小鼠中Ki67和N-钙黏蛋白阳性细胞的表达显著低于其对照组。
总之，结果表明LSZ通过PI3K/AKT/mTOR途径抑制结肠癌细胞的增殖、运动和EMT。
