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Surfactin induces apoptosis in human breast cancer MCF-7 cells through a ROS/JNK-mediated mitochondrial/caspase pathway.
Chem Biol Interact. 2010 Feb 12; 183(3):357-62.CB

Abstract

Surfactin has been known to inhibit proliferation and induce apoptosis in cancer cells. However, the molecular mechanisms involved in surfactin-induced apoptosis remain poorly understood. The present study was undertaken to elucidate the underlying network of signaling events in surfactin-induced apoptosis of human breast cancer MCF-7 cells. In this study, surfactin caused reactive oxygen species (ROS) generation and the surfactin-induced cell death was prevented by antioxidants N-acetylcysteine (NAC) and catalase, suggesting involvement of ROS generation in surfactin-induced cell death. Surfactin induced a sustained activation of the phosphorylation of ERK1/2 and JNK, but not p38. Moreover, surfactin-induced cell death was reversed by PD98059 (an inhibitor of ERK1/2) and SP600125 (an inhibitor of JNK), but not by SB203580 (an inhibitor of p38). However, the phosphorylation of JNK rather than ERK1/2 activation by surfactin was blocked by NAC/catalase. These results suggest that the action of surfactin on MCF-7 cells was via ERK1/2 and JNK, but not via p38, and the ERK1/2 and JNK activation induce apoptosis through two independent signaling mechanisms. Surfactin triggered the mitochondrial/caspase apoptotic pathway indicated by enhanced Bax-to-Bcl-2 expression ratio, loss of mitochondrial membrane potential, cytochrome c release, and caspase cascade reaction. The NAC and SP600125 blocked these events induced by surfactin. Moreover, the general caspase inhibitor z-VAD-FMK inhibited the caspase-6 activity and exerted the protective effect against the surfactin-induced cell death. Taken together, these findings suggest that the surfactin induces apoptosis through a ROS/JNK-mediated mitochondrial/caspase pathway.

Authors+Show Affiliations

Key Laboratory of Food Safety and Sanitation, Ministry of Education, College of Food Engineering and Biotechnology, Tianjin University of Science and Technology, Tianjin, China. wahwawayu@126.comNo 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

19954742

Citation

Cao, Xiao-hong, et al. "Surfactin Induces Apoptosis in Human Breast Cancer MCF-7 Cells Through a ROS/JNK-mediated Mitochondrial/caspase Pathway." Chemico-biological Interactions, vol. 183, no. 3, 2010, pp. 357-62.
Cao XH, Wang AH, Wang CL, et al. Surfactin induces apoptosis in human breast cancer MCF-7 cells through a ROS/JNK-mediated mitochondrial/caspase pathway. Chem Biol Interact. 2010;183(3):357-62.
Cao, X. H., Wang, A. H., Wang, C. L., Mao, D. Z., Lu, M. F., Cui, Y. Q., & Jiao, R. Z. (2010). Surfactin induces apoptosis in human breast cancer MCF-7 cells through a ROS/JNK-mediated mitochondrial/caspase pathway. Chemico-biological Interactions, 183(3), 357-62. https://doi.org/10.1016/j.cbi.2009.11.027
Cao XH, et al. Surfactin Induces Apoptosis in Human Breast Cancer MCF-7 Cells Through a ROS/JNK-mediated Mitochondrial/caspase Pathway. Chem Biol Interact. 2010 Feb 12;183(3):357-62. PubMed PMID: 19954742.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Surfactin induces apoptosis in human breast cancer MCF-7 cells through a ROS/JNK-mediated mitochondrial/caspase pathway. AU - Cao,Xiao-hong, AU - Wang,Ai-hua, AU - Wang,Chun-ling, AU - Mao,De-zhi, AU - Lu,Mei-fang, AU - Cui,Yun-qian, AU - Jiao,Run-zhi, Y1 - 2009/11/30/ PY - 2009/09/10/received PY - 2009/11/21/revised PY - 2009/11/23/accepted PY - 2009/12/4/entrez PY - 2009/12/4/pubmed PY - 2010/2/26/medline SP - 357 EP - 62 JF - Chemico-biological interactions JO - Chem Biol Interact VL - 183 IS - 3 N2 - Surfactin has been known to inhibit proliferation and induce apoptosis in cancer cells. However, the molecular mechanisms involved in surfactin-induced apoptosis remain poorly understood. The present study was undertaken to elucidate the underlying network of signaling events in surfactin-induced apoptosis of human breast cancer MCF-7 cells. In this study, surfactin caused reactive oxygen species (ROS) generation and the surfactin-induced cell death was prevented by antioxidants N-acetylcysteine (NAC) and catalase, suggesting involvement of ROS generation in surfactin-induced cell death. Surfactin induced a sustained activation of the phosphorylation of ERK1/2 and JNK, but not p38. Moreover, surfactin-induced cell death was reversed by PD98059 (an inhibitor of ERK1/2) and SP600125 (an inhibitor of JNK), but not by SB203580 (an inhibitor of p38). However, the phosphorylation of JNK rather than ERK1/2 activation by surfactin was blocked by NAC/catalase. These results suggest that the action of surfactin on MCF-7 cells was via ERK1/2 and JNK, but not via p38, and the ERK1/2 and JNK activation induce apoptosis through two independent signaling mechanisms. Surfactin triggered the mitochondrial/caspase apoptotic pathway indicated by enhanced Bax-to-Bcl-2 expression ratio, loss of mitochondrial membrane potential, cytochrome c release, and caspase cascade reaction. The NAC and SP600125 blocked these events induced by surfactin. Moreover, the general caspase inhibitor z-VAD-FMK inhibited the caspase-6 activity and exerted the protective effect against the surfactin-induced cell death. Taken together, these findings suggest that the surfactin induces apoptosis through a ROS/JNK-mediated mitochondrial/caspase pathway. SN - 1872-7786 UR - https://www.unboundmedicine.com/medline/citation/19954742/Surfactin_induces_apoptosis_in_human_breast_cancer_MCF_7_cells_through_a_ROS/JNK_mediated_mitochondrial/caspase_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0009-2797(09)00498-0 DB - PRIME DP - Unbound Medicine ER -