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The nuclear export of TR3 mediated gambogic acid-induced apoptosis in cervical cancer cells through mitochondrial dysfunction

机译:通过线粒体功能障碍,TR3介导的藤黄酸诱导宫颈癌细胞凋亡的核输出

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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.
机译:目前,化学疗法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使用,因此迫切需要开发用于宫颈癌的新药。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有待研究。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,藤黄酸诱导的凋亡需要TR3表达。在该机制中,藤黄酸促进TR3的核输出,从而导致p53的上调,从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的藤黄酸诱导的细胞凋亡。

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