Four novel Gelsemium elegans cyclic peptides (GEPs) were isolated in an antihuman cervical carcinoma activity tracking method, and their amino acid sequences were identified. The GEP-1 cyclic-(Trp-Leu-His-Val)-peptide inhibited HeLa cell proliferation in a dose- and time-dependent manner. GEP-1 induced intracellular reactive oxygen species (ROS) overproduction and induced HeLa cells apoptosis in a caspase-dependent manner. GEP-1 also induced collapse of the mitochondrial membrane potential and promoted the mitochondrial release of cytochrome c (cyt c), apoptosis-inducing factor (AIF), and endonuclease G (Endo G) in HeLa cells. Furthermore, GEP-1 triggered the extrinsic death receptor-dependent pathway, which was characterized by activating Fas and FADD. Notably, GEP-1 is a potential antihuman cervical carcinoma peptide.

中文翻译：

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Gelsemium elegans 环肽通过内在和外在途径诱导人宫颈癌细胞凋亡

四种小说线虫采用抗人宫颈癌活动追踪法分离环肽（GEPs）并鉴定其氨基酸序列。GEP-1 环状-(Trp-Leu-His-Val)-肽以剂量和时间依赖性方式抑制 HeLa 细胞增殖。GEP-1 以半胱天冬酶依赖性方式诱导细胞内活性氧 (ROS) 过度产生并诱导 HeLa 细胞凋亡。GEP-1 还诱导线粒体膜电位崩溃并促进 HeLa 细胞中细胞色素 c (cyt c)、凋亡诱导因子 (AIF) 和内切核酸酶 G (Endo G) 的线粒体释放。此外，GEP-1 触发了外在的死亡受体依赖性途径，其特征是激活 Fas 和 FADD。值得注意的是，GEP-1 是一种潜在的抗人宫颈癌肽。