Host defense peptide Hymenochirin-1B induces lung cancer cell apoptosis and cell cycle arrest through the mitochondrial pathway
Host defense peptide Hymenochirin-1B induces lung cancer cell apoptosis and cell cycle arrest through the mitochondrial pathway
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宿主防御肽Hymenochirin-1B通过线粒体途径诱导肺癌细胞凋亡和细胞周期停滞
DOI：
10.1016/j.bbrc.2019.03.029
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发表时间：
2019
影响因子：
3.1
通讯作者：
Yuchao Gu
中科院分区：
文献类型：
--
作者：
Yihan Zhang;Changning Sun;Guokai Xiao;Yuchao Gu
宿主防御肽Hymenochirin-1B的抗肿瘤活性已被广泛研究。然而，其机制仍然未知。在这项研究中，线性肽，Hymenochirin-1B，通过固相肽合成，并评估其抗癌疗效。结果发现Hymenochirin-1B可诱导肺癌细胞凋亡，并使细胞周期阻滞于G 0/G1期。此外，Hymenochirin-1B可以进入细胞并与线粒体共定位。Hymenochirin-1B处理后，NCI-H1299和A549细胞线粒体膜电位降低，活性氧增加，凋亡相关蛋白Bax/Bcl-2比值和活化的Caspase-3表达增加，提示Hymenochirin-1B通过线粒体途径诱导细胞凋亡。我们的研究结果为Hymenochirin-1B的抗癌机制提供了新的见解，这可能有助于其在未来进一步开发为抗癌药物。
The antineoplastic activity of host defense peptide Hymenochirin-1B, has been extensively studied. However, the mechanism still remains unknown. In this study, linear peptide, Hymenochirin-1B, was synthesized via solid-phase peptide synthesis and evaluated for its anticancer efficacy. We found Hymenochirin-1B induced lung cancer cell apoptosis and cell cycle arrest at the G0/G1 phase. Moreover, Hymenochirin-1B could enter the cells and colocalized with mitochondria. Furthermore, decrease of mitochondrial membrane potential, increase of reactive oxygen species and the expression of apoptosis-associated protein (Bax/Bcl-2 ratio and activated Caspase-3) were observed in NCI-H1299 and A549 cells after Hymenochirin-1B treatment, suggesting that Hymenochirin-1B induced apoptosis via mitochondrial pathway. Our results provide new insights on the anticancer mechanism of Hymenochirin-1B, which may contribute to its further development into an antineoplastic drug in the future.