Induction of apoptosis by VB1 in breast cancer cells: The role of reactive oxygen species and Bcl-2 family proteins

We have previously reported that the EVn-50 mixture of vitexins (lignan compounds) containing the purified vitexin (neolignan) compound, 6-hydroxy-4(4-hydroxy-3-methoxyphenyl)-3-hydroxymethyl-7-methoxy-3,4-dihydro-2-naphthaldehyde, termed VB1, exhibits potent anticancer activity through the inductio...

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Bibliographic Details
Published in:International journal of molecular medicine 2014-02, Vol.33 (2), p.423-430
Main Authors: LIU, LI-HUA, ZHOU, YING-JUN, DING, LAN, ZHANG, SHUN-ZHI, SUN, JI, CAO, JIAN-GUO
Format: Article
Language:English
Subjects:
Apoptosis
Bcl-2
Breast cancer
Care and treatment
Cytotoxicity
Genetic aspects
Medical prognosis
Physiological aspects
Physiology
Proteins
Reactive oxygen species
Risk factors
Rodents
Studies
Tumors
VB1
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Summary:We have previously reported that the EVn-50 mixture of vitexins (lignan compounds) containing the purified vitexin (neolignan) compound, 6-hydroxy-4(4-hydroxy-3-methoxyphenyl)-3-hydroxymethyl-7-methoxy-3,4-dihydro-2-naphthaldehyde, termed VB1, exhibits potent anticancer activity through the induction of apoptosis in several types of cancer cells, including MDA-MB-231 cells. However, the exact molecular mechanisms by which VB1 induces apoptosis in MDA-MB-231 cells have not yet been fully elucidated. In this study, to our knowledge, we provide for the first time mechanistic evidence that VB1-induced apoptosis in the human breast cancer line, MDA-MB-231, is associated with the generation of reactive oxygen species (ROS), the activation of caspases and the modulation of the expression of myeloid leukemia cell differentiation protein 1 (Mcl-1), B cell lymphoma-2 (Bcl-2) and Bcl-2-associated X (Bax) proteins. The silencing of Mcl-1 by RNA interference enhanced VB1-induced apoptosis. In addition, VB1 did not induce ROS generation or apoptosis in the immortalized non-cancerous breast cell line, MCF-10A. Our findings reveal a novel mechanism underlying VB1-induced apoptosis, and highlight VB1 as a promising candidate for the therapy of human breast cancer.
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.2013.1567