Latex of euphorbia antiquorum induces apoptosis in human cervical cancer cells via c-Jun N-terminal kinase activation and reactive oxygen species production

Wen Tsong Hsieh, Hui Yi Lin, Jou Hsuan Chen, Yueh Hsiung Kuo, Ming Jen Fan, Rick Sai Chuan Wu, King Chuen Wu, W. Gibson Wood, Jing Gung Chung

    Research output: Contribution to journalArticlepeer-review

    18 Scopus citations

    Abstract

    Latex of Euphorbia antiquorum (EA) has inhibitory effects on several different cancer cell lines. However, the molecular mechanism of EA inhibitory effects on human cervical cancer HeLa cell growth has not been explored. EA induced apoptosis, which was characterized by morphological change, DNA fragmentation, increased sub-G1 population, and alterations in levels of apoptosis-associated proteins. Treatment with EA increased cell death and expression levels of caspase-8, -9, and -3. EA suppressed expression of Bcl-2, increased Bax, and reduced cleavage of Bid and the translocation of tBid to the mitochondria and the release of cytochrome c from mitochondria. EA caused a loss of mitochondrial membrane potential (Δ Ψ m) and an increase in cellular reactive oxygen species (ROS). EA-induced ROS formation was suppressed by cyclosporine A (an inhibitor of the Δ Ψ m) or allopurinol (an effective scavenger of ROS). EA also increased expression of Fas, FasL, and c-Jun N-terminal kinase (JNK), p38, and mitogen-activated protein kinase (MAPK) and decreased expression of extracellular signal-regulated kinase (ERK) 1/2-p. Co-treatment with the JNK inhibitor SP600125 inhibited EA-induced apoptosis and the activation of caspase-8, -9, and -3. Results of this study provide support for the hypothesis that EA causes cell death via apoptotic pathways in human cervical adenocarcinoma HeLa cells.

    Original languageEnglish (US)
    Pages (from-to)1339-1347
    Number of pages9
    JournalNutrition and cancer
    Volume63
    Issue number8
    DOIs
    StatePublished - Nov 1 2011

    ASJC Scopus subject areas

    • Medicine (miscellaneous)
    • Oncology
    • Nutrition and Dietetics
    • Cancer Research

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