NDLI: Combined treatment with verrucarin A and tumor necrosis factor- sensitizes apoptosis by overexpression of nuclear factor-kappaB-mediated Fas.

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Combined treatment with verrucarin A and tumor necrosis factor- sensitizes apoptosis by overexpression of nuclear factor-kappaB-mediated Fas.

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Combined treatment with verrucarin A and tumor necrosis factor- sensitizes apoptosis by overexpression of nuclear factor-kappaB-mediated Fas.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Jayasooriya, Rajapaksha Gedara Prasad Tharanga Moon, Dong-Oh Park, Sang Rul Choi, Yung Hyun Asami, Yukihiro Kim, Mun-Ock Jang, Jae-Hyuk Kim, Bo Yeon Ahn, Jong Seog Kim, Gi-Young
Description	Author Affiliation: Jayasooriya RG ( Laboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, Ara-1 dong, Jeju 690-756, Republic of Korea.)
Abstract	Verrucarin A (VA) is a member of the family of macrocyclic trichothecenes, which exhibit anti-cancer and immune-modulating activities. However, VA has not yet been demonstrated to be involved in the sensitization of tumor necrosis factor-alpha (TNF- )-mediated apoptosis. In the present study, we found that VA triggers TNF- -induced apoptosis in human breast cancer MDA-MB-231 and MCF-7 cells. In particular, activation of caspas-3 and caspase-8 as well as release of cytochrome c were significantly enhanced in response to the combined treatment with VA and TNF- (VA/TNF- ) and the pan-caspase inhibitor z-VAD-fmk completely reversed the apoptosis, suggesting that caspases are the main effector molecules in VA/TNF- -induced apoptosis via the intrinsic and extrinsic pathway. Moreover, we confirmed that enhanced Fas expression plays a critical role, because the Fas-blocking antibody partially inhibited VA/TNF- -induced apoptosis. VA also increased specific DNA-binding activity of nuclear factor-kappaB (NF-κB) via nuclear translocation of p50 and p65. In addition, pretreatment with the NF-κB inhibitor MG132 blocked VA/TNF- -induced apoptosis by suppression of NF-κB-dependent Fas expression. These results indicated that VA enhances TNF- -induced apoptosis via NF-κB-dependent Fas overexpression.
File Format	HTM / HTML
ISSN	13826689
Issue Number	2
Volume Number	36
e-ISSN	18727077
Journal	Environmental Toxicology and Pharmacology
Language	English
Publisher	Elsevier
Publisher Date	2013-09-01
Publisher Place	Netherlands
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Environmental Health Discipline Pharmacology Antigens, Cd95 Metabolism Antineoplastic Combined Chemotherapy Protocols Pharmacology Apoptosis Drug Effects Breast Neoplasms Nf-kappa B Active Transport, Cell Nucleus Antibodies Antagonists & Inhibitors Pathology Caspase 3 Caspase 8 Caspase Inhibitors Cytochromes c Dose-response Relationship, Drug Female Humans Mcf-7 Cells Nf-kappa B P50 Subunit Signal Transduction Time Factors Transcription Factor Rela Trichothecenes Tumor Necrosis Factor-alpha Up-regulation Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Medicine Toxicology Pharmacology

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