Paclitaxel induces apoptosis of esophageal squamous cell carcinoma cells by downregulating STAT3 phosphorylation at Ser727
Paclitaxel induces apoptosis of esophageal squamous cell carcinoma cells by downregulating STAT3 phosphorylation at Ser727
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紫杉醇通过下调STAT3 Ser727磷酸化诱导食管鳞癌细胞凋亡
DOI：
10.3892/or.2017.5503
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发表时间：
2017-04-01
期刊：
影响因子：
4.2
通讯作者：
Liu, Yongzhang
中科院分区：
文献类型：
--
作者：
Zhang, Xiaolong;Wu, Xiaoyi;Liu, Yongzhang
紫杉醇可诱导多种癌细胞凋亡。然而，紫杉醇诱导人食管鳞状细胞癌（ESCC）细胞凋亡的机制仍有待明确。在这项研究中，我们发现紫杉醇通过下调信号转导和转录激活剂3（STAT3）和磷酸化STAT3（Ser727）来增加相关凋亡蛋白的表达和细胞色素c的释放，从而诱导细胞凋亡。此外，紫杉醇处理ESCC细胞EC -1和Eca-109导致明显的线粒体膜电位去极化和活性氧的显着增加。此外，紫杉醇治疗导致线粒体呼吸的抑制。总之，我们的研究结果表明紫杉醇通过降低 STAT3 和磷酸化 STAT3 (Ser727) 水平诱导 EC -1 和 Eca-109 细胞凋亡，并表明紫杉醇可能通过诱导 ESCC 细胞线粒体凋亡而具有治疗 ESCC 的治疗潜力。
Paclitaxel induces apoptosis in a variety of cancer cells. However, the mechanism of paclitaxel inducing apoptosis in human esophageal squamous cell carcinoma (ESCC) remains to be defined. In this study, we found that paclitaxelinduced apoptosis by increasing the relevant apoptosis protein expression and the release of cytochrome c via downregulation of signal transducer and activator of transcription 3 (STAT3) and phospho-STAT3 (Ser727). In addition, paclitaxel treatment of ESCC cells EC -1 and Eca-109 led to marked mitochondrial membrane potential depolarization and significantly increasing of reactive oxygen species. Moreover, paclitaxel treatment resulted in the inhibition of mitochondrial respiration. In conclusion, our findings reveal that paclitaxel induced apoptosis in both EC -1 and Eca-109 cells through the reduction of STAT3 and phospho-STAT3 (Ser727) level, and suggest that paclitaxel may be of therapeutic potential in the treatment of ESCC through the induction of mitochondrial apoptosis in ESCC cells.