Zhang Chunhong, Liu Jia, Tao Fengxing, Lu Yiyi, He Qin, Zhao Liang, Ou Rongying, Xu Yunsheng, Li Wenfeng
Department of Pharmacy, The First Affliated Hospital of Wenzhou Medical University Wenzhou Zhejiang Province China.
Department of Dermatovenereology, The First Affliated Hospital of Wenzhou Medical University Nanbaixiang Street Wenzhou Zhejiang Province China
RSC Adv. 2019 Apr 16;9(21):11855-11864. doi: 10.1039/c8ra10542a. eCollection 2019 Apr 12.
At present, chemotherapy is still the main treatment for cervical cancer. However, the drug resistance of chemotherapy drugs seriously restricts its use, so it is urgent to develop new drugs for cervical cancer. Some studies have shown that gambogic acid has a strong anti-tumor effect, while the anti-tumor effect and molecular mechanism of gambogic acid on cervical cancer need to be studied. Our study confirms that the cytotoxic effect of gambogic acid on cervical cancer cells depends on the expression of TR3 protein. Moreover, gambogic acid-induced apoptosis requires TR3 expression. In the mechanism, gambogic acid promoted nuclear export of TR3, resulting in up-regulation of p53, which leads to the decrease of mitochondrial membrane potential, eventually inducing apoptosis. These results suggest that the nuclear export of TR3 mediated gambogic acid-induced apoptosis through a p53-dependent apoptosis pathway.
目前,化疗仍是宫颈癌的主要治疗方法。然而,化疗药物的耐药性严重限制了其应用,因此迫切需要开发针对宫颈癌的新药。一些研究表明,藤黄酸具有很强的抗肿瘤作用,而藤黄酸对宫颈癌的抗肿瘤作用及其分子机制尚需研究。我们的研究证实,藤黄酸对宫颈癌细胞的细胞毒性作用取决于TR3蛋白的表达。此外,藤黄酸诱导的细胞凋亡需要TR3表达。在机制上,藤黄酸促进TR3的核输出,导致p53上调,进而导致线粒体膜电位降低,最终诱导细胞凋亡。这些结果表明,TR3的核输出通过p53依赖性凋亡途径介导藤黄酸诱导的细胞凋亡。