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雷公藤红素通过 MAPK/ERK 信号通路抑制食管鳞癌细胞的增殖和迁移。

Triptolide prevents proliferation and migration of Esophageal Squamous Cell Cancer via MAPK/ERK signaling pathway.

机构信息

Department of Pathology, Shanxi Medical University, Taiyuan, Shanxi 030001, PR China; Shanxi Key Laboratory of Carcinogenesis and Translational Research of Esophageal Cancer, Shanxi Medical University, Taiyuan, Shanxi 030001, PR China; Key Laboratory of Cellular Physiology, Ministry of Education, Shanxi Medical University, Taiyuan, Shanxi 030001, PR China.

Department of Pathology, Shanxi Medical University, Taiyuan, Shanxi 030001, PR China; Shanxi Key Laboratory of Carcinogenesis and Translational Research of Esophageal Cancer, Shanxi Medical University, Taiyuan, Shanxi 030001, PR China; Key Laboratory of Cellular Physiology, Ministry of Education, Shanxi Medical University, Taiyuan, Shanxi 030001, PR China.

出版信息

Eur J Pharmacol. 2019 May 15;851:43-51. doi: 10.1016/j.ejphar.2019.02.030. Epub 2019 Feb 16.

DOI:10.1016/j.ejphar.2019.02.030
PMID:30779917
Abstract

Triptolide, the component of traditional Chinese herb, has been used as an inflammatory medicine and reported to be anti-tumor for various cancers recently. However, the effect of triptolide on Esophageal Squamous Cell Cancer (ESCC) has not yet been elucidated. In the study, we found that triptolide significantly inhibited cell proliferation, invasion, migration and survivability of ESCC cells. Moreover, we observed that triptolide induced ESCC cell cycle arrest at the G1/S phase and apoptosis through cyclin D1-CDK4/6 regulation and caspases activation. In addition, we revealed that triptolide regulates cell apoptosis and metastasis by p53 and mitogen-activated protein kinases/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway, respectively. Meanwhile, the inhibitory effect of triptolide on ESCC was validated in mouse xenograft model. So, we propose that triptolide may be a candidate drug for ESCC.

摘要

雷公藤红素是一种传统中药的成分,最近被用作抗炎药物,并被报道对各种癌症具有抗肿瘤作用。然而,雷公藤红素对食管鳞癌(ESCC)的作用尚未阐明。在本研究中,我们发现雷公藤红素可显著抑制 ESCC 细胞的增殖、侵袭、迁移和存活能力。此外,我们观察到雷公藤红素通过调节细胞周期蛋白 D1-CDK4/6 和激活半胱天冬酶诱导 ESCC 细胞周期停滞在 G1/S 期和凋亡。此外,我们揭示雷公藤红素通过 p53 和丝裂原活化蛋白激酶/细胞外信号调节激酶(MAPK/ERK)信号通路分别调节细胞凋亡和转移。同时,在小鼠异种移植模型中验证了雷公藤红素对 ESCC 的抑制作用。因此,我们提出雷公藤红素可能是 ESCC 的候选药物。

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