Genistein anticancer activity

Genistein has been considered the primary anticancer constituent in soy, based on putative in vitro activities that include its ability to inhibit topoisomerase I and II activity, inhibit protein tyrosine phosphorylation, induce differentiation of cancer cell lines, and act as an estrogen agonist. 

Genistein has been used for years as a model inhibitor of protein tyrosine kinases (PTKs). This ubiquitous enzyme, which is also present in thyroid foUicular ceUs, is involved in phosphorylation of tyrosyl residues of membrane-bound receptors leading to signal transduction. One of the signal transduction cascades leads to topoisomerase II, which participates in DNA replication. Blocking PTK activity is one of the mechanisms believed to be responsible for the anticancer potential of genistein. For reviews addressing this issue, which are beyond the scope of this chapter, see Peterson (1995), and Ravindranath et al (2004). 

The predominant effect of flavonoid and isoflavonoid supplementation in ex vivo cell culture models appears to be one of promoting apoptosis [54—57]. This is repeatedly observed in studies witti transformed cancer cells, leading to the descriptions cytoprotective and/or chemopreventive [6,58]. Two poly-phenolic compounds that have been extensively studied in anticancer research are quercetin and genistein, a flavonoid and isoflavone, respectively. However, ex vivo studies with primary cultured cells in 2000 and 2001 showed that some flavonoids can prevent apoptosis promoted by agents that induce oxidative stress [7,8,59]. The outcome of flavonoid treatment is expected to show a complex dependence on a number of factors, including the type of flavonoid, its concentration, the type of cell (e.g., transformed versus nontransformed), the mechanisms of action of the flavonoid, the nature of the proapoptotic stimulus, and the specific apoptotic signaling pathway that is activated. 

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