Anti-oncogenes tumor- suppressor genes

Although the exact mechanism responsible for the proapoptotic effects of capsaicin remains unknown, several different mechanisms have been proposed, including the inhibition of plasma membrane nicotinamide adenine dinucleotide reduced (NADH) oxidase activity [121], regulation by Bcl-2 and calcineurin [122], and the overexpression of the p53 tumor suppressor gene and/or c-myc proto-oncogene [123]. Since tumor promotion is related to inflammation, the anti-inflammatory and anti-tumoral effects of capsaicin are most likely directly related to each other and are thus both of interest. In addition, the activation of NF-kB by... 

Apoptosis resistance in cancer is mediated by diverse mechanisms that act at different points of the cell death pathway, leading to its disruption. Many of the responsible molecules have been identified and con5)rise potential targets for therapeutic intervention (Nicholson 2000). They can be divided into two major classes (a) oncogenes with anti-apoptotic activities, which are frequently over-expressed due to transactivation or post-transcriptional regulation and (b) tumor suppressor genes with pro-apoptotic capabilities. In addition, death receptor signaling can be dampened by the expression of inactive decoy receptors on the cell surface (Ashkenazi 2002). 

Nuclear tumor suppressors inhibit return to the cell cycle in fully differentiated cells. The genes that code for these proteins are referred to as anti-oncogenes due to this function. On the role of p53 and pRb, see p.394. 

Apoptosis induced by doxorabicin is accompanied by the down-regulation of the expression of the oncogene proteins c-erb-2 and c-myc, the anti-apoptotic gene proteins (bcl-2), p53 tumor suppressor protein, and up-iegnlation of the expression of PCNA and c-fos. 

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