解剖学报 ›› 2025, Vol. 56 ›› Issue (1): 4-10.doi: 10.16098/j.issn.0529-1356.2025.01.001

• 肿瘤学专栏 •    下一篇

雷公藤甲素下调CT26结肠癌细胞保罗样蛋白激酶-1水平发挥抑瘤活性

卢智豪 李雪铭 姜艳玲 赵旭 冯婧 李健*   

  1. 北京中医药大学中医学院组织学胚胎学教研室,北京100029
  • 收稿日期:2024-04-16 修回日期:2024-07-16 出版日期:2025-02-06 发布日期:2025-02-06
  • 通讯作者: 李健 E-mail:lijiancn922@126.com
  • 基金资助:

Effect of triptolide on the expression of Polo-like kinase -1 in CT26 colon cancer and its antitumor activity

LU Zhi-hao LI Xue-ming JIANG Yan-ling ZHAO Xu FENG Jing LI Jian*   

  1. Histology and Embryology Department, School of Traditional Chinese Medicine, Beijing University of Traditional Chinese Medicine, Beijing 100029, China
  • Received:2024-04-16 Revised:2024-07-16 Online:2025-02-06 Published:2025-02-06
  • Contact: LI Jian E-mail:lijiancn922@126.com

摘要:

目的 探讨雷公藤甲素抗CT26结肠癌及其对保罗样蛋白激酶-1(PLK-1)蛋白表达的影响。方法清洁级BALB/c小鼠40只,每只小鼠移植1×106个CT26细胞到右前肢背侧皮下,建立荷瘤小鼠模型,并随机分4组,即肿瘤模型组(溶剂对照)、阳性药组[奥沙利铂,5mg/(kg·d)]、雷公藤甲素低剂量组[50μg/(kg·d)]和雷公藤甲素高剂量组[100μg/(kg·d)],腹腔注射给药(隔日1次,共10次)。同时评估药物体外作用对CT26细胞增殖、迁移、侵袭及有丝分裂的影响。结果雷公藤甲素能显著抑制CT26结肠癌细胞增殖、迁移和侵袭,干扰肿瘤细胞有丝分裂前期中心体分离和染色体正确排布;雷公藤甲素和PLK-1蛋白结合能为-7.1 kcal/mol,其能下调CT26细胞内PLK-1的表达。结论雷公藤甲素通过下调PLK-1的表达发挥抗CT26结肠癌的药理作用。

关键词: 雷公藤甲素, CT26细胞系, 移植瘤模型, 保罗样蛋白激酶-1, 免疫组织化学, 小鼠

Abstract:

Objective To investigate the antitumor effects of triptolide against CT26 colon cancer and its impact on the expression of Polo-like kinase-1 (PLK-1) protein.  Methods  Forty clean grade BALB/c mice, each mouse was implanted with 1×106 CT26 cells into the dorsal side of the right forelimb to establish a tumor-bearing mouse model. Experimental animals were randomly divided into four groups, the tumor model group (saline control), the positive drug group [oxaliplatin, 5mg/(kg·d)], the low-dose triptolide group [50μg/(kg·/d)], and the high-dose triptolide group [100μg/(kg·d)]. The drugs were administered through intraperitoneal injection (10 times in total, once every other day). The in vitro effects of the drugs on the proliferation, migration, invasion, and mitosis of CT26 cells were also assessed.   Results  Triptolide significantly inhibited the proliferation, migration, and invasion of CT26 colon cancer cells, and disrupted the separation of centrosomes and the correct arrangement of chromosomes during the prophase of mitosis in tumor cells. The binding energy of triptolide and PLK-1 protein was -7.1 kcal/mol, and it could down-regulate the expression of PLK-1 in CT26 cells.  Conclusion  Triptolide exerts its antitumor effects against CT26 colon cancer by downregulating the expression of PLK-1.

Key words:  Triptolide, CT26 cell line, Tumor-bearing model, Polo-like kinase-1, Immunohistochemistry,  , Mouse



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