Proteomic analysis reveals that pardaxin triggers apoptotic signaling pathways in human cervical carcinoma HeLa cells: Cross talk among the UPR, c-Jun and ROS

Tsui Chin Huang, Jyh Yih Chen

研究成果: 雜誌貢獻文章

20 引文 斯高帕斯(Scopus)

摘要

Pardaxin, an antimicrobial peptide secreted by the Red Sea flatfish Pardachirus marmoratus, inhibits proliferation and induces apoptosis of human cancer cell lines. However, the underlying molecular mechanisms are only partially understood at present. In this study, we used proteomic approaches and network reconstruction to clarify the mechanism of pardaxin-induced apoptosis in human cervical carcinoma HeLa cells. We identified that pardaxin-regulated proteins predominantly function in the unfolded protein response, oxidative stress and cytoskeletal distribution. Molecular examination of signal transduction and cellular localization demonstrated that the activator protein-1 transcription factor was activated, which eventually caused apoptosis via both caspase-and apoptosis-inducing factor-dependent pathways. Scavenging of reactive oxygen species (ROS) alleviated c-Jun activation, and small interfering RNA knockdown of c-Jun abrogated pardaxin-induced caspase activation and cell death, thereby implicating ROS and c-Jun in pardaxin-induced apoptosis signaling. In summary, this study provides the first proteininteracting network maps and novel insights into the biological responses and potential toxicity of pardaxin.
原文英語
頁(從 - 到)1833-1842
頁數10
期刊Carcinogenesis
34
發行號8
DOIs
出版狀態已發佈 - 八月 2013

ASJC Scopus subject areas

  • Cancer Research

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