Tags

Type your tag names separated by a space and hit enter

Latex of Euphorbia antiquorum induces apoptosis in human cervical cancer cells via c-jun n-terminal kinase activation and reactive oxygen species production.
Nutr Cancer. 2011 Nov; 63(8):1339-47.NC

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 (ΔΨm) and an increase in cellular reactive oxygen species (ROS). EA-induced ROS formation was suppressed by cyclosporine A (an inhibitor of the ΔΨm) 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.

Authors+Show Affiliations

Department of Pharmacology, China Medical University, Taichung, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22044063

Citation

Hsieh, Wen-Tsong, et al. "Latex of Euphorbia Antiquorum Induces Apoptosis in Human Cervical Cancer Cells Via C-jun N-terminal Kinase Activation and Reactive Oxygen Species Production." Nutrition and Cancer, vol. 63, no. 8, 2011, pp. 1339-47.
Hsieh WT, Lin HY, Chen JH, et al. Latex of Euphorbia antiquorum induces apoptosis in human cervical cancer cells via c-jun n-terminal kinase activation and reactive oxygen species production. Nutr Cancer. 2011;63(8):1339-47.
Hsieh, W. T., Lin, H. Y., Chen, J. H., Kuo, Y. H., Fan, M. J., Wu, R. S., Wu, K. C., Wood, W. G., & Chung, J. G. (2011). Latex of Euphorbia antiquorum induces apoptosis in human cervical cancer cells via c-jun n-terminal kinase activation and reactive oxygen species production. Nutrition and Cancer, 63(8), 1339-47. https://doi.org/10.1080/01635581.2011.608481
Hsieh WT, et al. Latex of Euphorbia Antiquorum Induces Apoptosis in Human Cervical Cancer Cells Via C-jun N-terminal Kinase Activation and Reactive Oxygen Species Production. Nutr Cancer. 2011;63(8):1339-47. PubMed PMID: 22044063.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Latex of Euphorbia antiquorum induces apoptosis in human cervical cancer cells via c-jun n-terminal kinase activation and reactive oxygen species production. AU - Hsieh,Wen-Tsong, AU - Lin,Hui-Yi, AU - Chen,Jou-Hsuan, AU - Kuo,Yueh-Hsiung, AU - Fan,Ming-Jen, AU - Wu,Rick Sai-Chuan, AU - Wu,King-Chuen, AU - Wood,W Gibson, AU - Chung,Jing-Gung, Y1 - 2011/11/01/ PY - 2011/11/3/entrez PY - 2011/11/3/pubmed PY - 2012/3/20/medline SP - 1339 EP - 47 JF - Nutrition and cancer JO - Nutr Cancer VL - 63 IS - 8 N2 - 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 (ΔΨm) and an increase in cellular reactive oxygen species (ROS). EA-induced ROS formation was suppressed by cyclosporine A (an inhibitor of the ΔΨm) 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. SN - 1532-7914 UR - https://www.unboundmedicine.com/medline/citation/22044063/Latex_of_Euphorbia_antiquorum_induces_apoptosis_in_human_cervical_cancer_cells_via_c_jun_n_terminal_kinase_activation_and_reactive_oxygen_species_production_ L2 - https://www.tandfonline.com/doi/full/10.1080/01635581.2011.608481 DB - PRIME DP - Unbound Medicine ER -