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

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1833-1842
Number of pages10
JournalCarcinogenesis
Volume34
Issue number8
DOIs
Publication statusPublished - Aug 2013

ASJC Scopus subject areas

  • Cancer Research

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