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藤黄酸通过调节p65活性抑制卵巢癌肿瘤生长。

Gambogic acid inhibits the growth of ovarian cancer tumors by regulating p65 activity.

作者信息

Tang Qiusha, Lu Mudan, Zhou Huan, Chen Daozhen, Liu Lu

机构信息

Department of Pathology and Pathophysiology, Medical College, Southeast University, Nanjing, Jiangsu 210096, P.R. China.

Genetic Laboratory, Wuxi Hospital for Maternal and Child Health Care, The Affiliated Hospital of Nanjing Medical University, Wuxi, Jiangsu 214002, P.R. China.

出版信息

Oncol Lett. 2017 Jan;13(1):384-388. doi: 10.3892/ol.2016.5433. Epub 2016 Nov 24.

Abstract

Ovarian cancer patients often have poor prognosis, therefore, it is important to search for more effective therapeutic strategies to treat them. Gambogic acid (GA) exhibits an anti-tumor effect through various mechanisms, and has multiple targets in tumor cells. The present study aimed to elucidate the efficacy of GA in the treatment of ovarian cancer both and by analyzing its impact on cell survival and tumor growth through cell cycle and apoptosis analysis. GA inhibited the growth of ovarian cancer cells in a dose and time dependent manner, and arrested the cell cycle in ovarian cancer cells. Furthermore, GA increased caspase-3 and caspase-9 activity and inhibited RELA/NF-κB p65 (p65) DNA binding activity. Finally, GA suppressed tumor growth . Therefore, the current study suggests that GA inhibits the growth of ovarian cancer by regulating p65 activity, and may be developed as a novel therapeutic strategy to treat ovarian cancer.

摘要

卵巢癌患者的预后通常较差,因此,寻找更有效的治疗策略来治疗他们非常重要。藤黄酸(GA)通过多种机制发挥抗肿瘤作用,并且在肿瘤细胞中有多个靶点。本研究旨在通过细胞周期和凋亡分析,分析GA对细胞存活和肿瘤生长的影响,从而阐明GA在治疗卵巢癌方面的疗效。GA以剂量和时间依赖性方式抑制卵巢癌细胞的生长,并使卵巢癌细胞的细胞周期停滞。此外,GA增加了caspase-3和caspase-9的活性,并抑制了RELA/NF-κB p65(p65)的DNA结合活性。最后,GA抑制了肿瘤生长。因此,当前研究表明,GA通过调节p65活性来抑制卵巢癌的生长,并且可能被开发为一种治疗卵巢癌的新型治疗策略。

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