橙皮素通过调节DNA损伤/自噬途径抑制膀胱尿路上皮癌细胞增殖。
Pectolinarigenin inhibits bladder urothelial carcinoma cell proliferation by regulating DNA damage/autophagy pathways.
作者信息
Deng Zhao, Shen Dexin, Yu Mengxue, Zhou Fenfang, Shan Danni, Fang Yayun, Jin Wan, Qian Kaiyu, Li Shenjuan, Wang Gang, Zhang Yi, Ju Lingao, Xiao Yu, Wang Xinghuan
机构信息
Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Department of Biological Repositories, Zhongnan Hospital of Wuhan University, Wuhan, China.
出版信息
Cell Death Discov. 2023 Jul 1;9(1):214. doi: 10.1038/s41420-023-01508-9.
Pectolinarigenin (PEC), an active compound isolated from traditional herbal medicine, has shown potential anti-tumor properties against various types of cancer cells. However, its mechanism of action in bladder cancer (BLCA), which is one of the fatal human carcinomas, remains unexplored. In this study, we first revealed that PEC, as a potential DNA topoisomerase II alpha (TOP2A) poison, can target TOP2A and cause significant DNA damage. PEC induced G2/M phase cell cycle arrest via p53 pathway. Simultaneously, PEC can perform its unique function by inhibiting the late autophagic flux. The blocking of autophagy caused proliferation inhibition of BLCA and further enhanced the DNA damage effect of PEC. In addition, we proved that PEC could intensify the cytotoxic effect of gemcitabine (GEM) on BLCA cells in vivo and in vitro. Summarily, we first systematically revealed that PEC had great potential as a novel TOP2A poison and an inhibitor of late autophagic flux in treating BLCA.
芹菜素(PEC)是从传统草药中分离出的一种活性化合物,已显示出对多种癌细胞具有潜在的抗肿瘤特性。然而,其在膀胱癌(BLCA)(一种致命的人类癌症)中的作用机制仍未被探索。在本研究中,我们首先发现,作为一种潜在的DNA拓扑异构酶IIα(TOP2A)毒素,PEC可以靶向TOP2A并导致显著的DNA损伤。PEC通过p53途径诱导G2/M期细胞周期阻滞。同时,PEC可以通过抑制晚期自噬流来发挥其独特功能。自噬的阻断导致BLCA增殖受到抑制,并进一步增强了PEC的DNA损伤作用。此外,我们证明PEC可以在体内和体外增强吉西他滨(GEM)对BLCA细胞的细胞毒性作用。总之,我们首次系统地揭示了PEC作为一种新型TOP2A毒素和晚期自噬流抑制剂在治疗BLCA方面具有巨大潜力。