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

Abstract:

: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.

journal_name

Int J Mol Med

authors

Liu LH,Zhou YJ,Ding L,Zhang SZ,Sun J,Cao JG

doi

10.3892/ijmm.2013.1567

subject

Has Abstract

pub_date

2014-02-01 00:00:00

pages

423-30

issue

2

eissn

1107-3756

issn

1791-244X

journal_volume

33

pub_type

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