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 journalArticle

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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.

LanguageEnglish (US)
Pages1339-1347
Number of pages9
JournalNutrition and cancer
Volume63
Issue number8
DOIs
StatePublished - Nov 1 2011

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Euphorbia
JNK Mitogen-Activated Protein Kinases
Latex
Uterine Cervical Neoplasms
Reactive Oxygen Species
Apoptosis
Caspase 9
Caspase 8
HeLa Cells
Mitochondria
Cell Death
Allopurinol
Mitogen-Activated Protein Kinase 3
Mitochondrial Membrane Potential
Mitogen-Activated Protein Kinase 1
p38 Mitogen-Activated Protein Kinases
DNA Fragmentation
Cytochromes c
Cyclosporine
Cause of Death

ASJC Scopus subject areas

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

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Latex of euphorbia antiquorum induces apoptosis in human cervical cancer cells via c-Jun N-terminal kinase activation and reactive oxygen species production. / Hsieh, Wen-Tsong; Lin, Hui Yi; Chen, Jou Hsuan; Kuo, Yueh Hsiung; Fan, Ming Jen; Wu, Rick Sai Chuan; Wu, King Chuen; Wood, W. Gibson; Chung, Jing-Gung.

In: Nutrition and cancer, Vol. 63, No. 8, 01.11.2011, p. 1339-1347.

Research output: Contribution to journalArticle

Hsieh, Wen-Tsong ; Lin, Hui Yi ; Chen, Jou Hsuan ; Kuo, Yueh Hsiung ; Fan, Ming Jen ; Wu, Rick Sai Chuan ; Wu, King Chuen ; Wood, W. Gibson ; Chung, Jing-Gung. / Latex of euphorbia antiquorum induces apoptosis in human cervical cancer cells via c-Jun N-terminal kinase activation and reactive oxygen species production. In: Nutrition and cancer. 2011 ; Vol. 63, No. 8. pp. 1339-1347.
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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.",
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