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. Author manuscript; available in PMC: 2010 Feb 10.
Published in final edited form as: Cancer Epidemiol Biomarkers Prev. 2007 Mar 2;16(3):392. doi: 10.1158/1055-9965.EPI-06-1081

Figure 1. Mechanisms of apoptosis and growth arrest by isothiocyanates.

Figure 1

Isothiocyanates induce apoptosis and growth arrest involving a number of mechanisms, which may be particularly relevant in preventing lymphomagenesis and other neoplasms. Some potential mechanisms may involve their ability to inhibit the anti-apoptotic proteins, Bcl-2 and Bcl-x, and up-regulate the pro-apoptotic molecules, Bax and Bak, initiating apoptotic cell death through cytochrome c release and the subsequent activation of caspases. Isothiocyanates also can promote apoptotic cell death through the up-regulation of c-Jun N-terminal kinase (JNK) and down-regulation of nuclear factor (NF)-κB signaling pathways. These compounds also may induce cell cycle arrest by the induction of activator protein 1 (AP-1) resulting in up-regulation of the cyclin-dependent kinase (CDK) inhibitor, p21, and subsequent G(2)/M arrest.