Anticancer activity

Cancers can be defined as diseases in which unremitting clonal expansion of somatic cells kills by invading, subverting, and eroding normal tissues (Evan and Vousden, 2001). It has been documented that apoptosis (programmed cell death) is a key process in cancer development and progression. Inactivation of apoptosis is considered to be one of the six fundamental hallmarks of cancer, and therefore, apoptosis is a major target of cancer therapy development (Brown and Attardi, 2005). Hence, developing novel molecules that promote apoptosis by targeting both the intrinsic and extrinsic apoptotic pathways may lead to the development of effective cancer therapies.

Fucoxanthin is known to be important free-radical scavengers and antioxidants for the prevention of oxidative damage, which is an important contributor in carcinogenesis. Therefore, it might be suggested that fucoxanthin has potent capacities for new anticancer product developments in the food industries as well as in pharmaceuticals as novel chemopreventing agents for cancer therapy.

Exciting research studies have been published regarding carotenoids and its anticancer qualities. Ishikawa et al. showed anti-adult T-cell leukemia effects of fucoxanthin and its deacetylated metabolite, fucoxanthinol (Ishikawa et al., 2008). The inhibitory activities of fucoxanthin and fucox-anthinol were stronger than those of p-carotene and astaxanthin. Adult T-cell leukemia is a fatal malignancy of T lymphocytes caused by human T-cell leukemia virus type 1 infection and remains incurable. Therefore, carotenoids could be potentially useful therapeutic agents for adult T-cell leukemia patients. A recent study from Japan demonstrates that anticancer activity of fucoxanthin goes way beyond its ability to induce apopto-sis. Apoptosis inducing effect of fucoxanthin on human leukemia cells (HL-60) has been reported (Hosokawa et al., 1999; Kotake Nara et al., 2005b). The apoptosis induction was associated with activation of cas-pase-3, -8, and -9 which can be thought of as central executioner of the apoptotic pathway (Hengartner, 2000). Very recently, Ganesan et al. reported that siphonaxanthin derived from Codium fragile is a more potent growth inhibitor against HL-60 cells than fucoxanthin (Ganesan et al., 2011). The structural differences between these two carotenoids are fuco-xanthin contains epoxide and an allenic bond in its structure, whereas siphonaxanthin does not contain those functional groups; however, sipo-naxanthin has an additional hydroxyl group on the 19th carbon atom. Since esterified form of siphonaxanthin showed lower inhibitory effect, it is suggested that the presence of hydroxyl group is contributed to the strong inhibitory effect of siphonaxanthin (Ganesan et al., 2011). Meanwhile, antiproliferative effect and apoptosis induction by fucoxanthin in human colon cancer cells (Caco-2, HT-29, and DLD-1) were observed by

Hosokawa et al. (2004). Fucoxanthin remarkably reduced the viability of human colon cancer cell lines and treatment with fucoxanthin induced DNA fragmentation. Exposure to fucoxanthin decreased the level of apoptosis-suppressing protein (Bcl-2), which suggest that anticancer activity of fucoxanthin were mainly caused by apoptosis. Apoptosis-inducing effect of fucoxanthin in human prostate cancer cells (PC-3, DU 145, and LNCaP) has also been observed (Kotake Nara et al., 2001, 2005a). Although current knowledge of relationship between the structure and apoptosis activity of the fucoxanthin is limited, some researchers suggest that conjugated double bonds and 5,6-monoepoxide are thought to be highly susceptible to acids, alkali and oxygen lead to their prooxidant actions which might cause apoptosis induction in the several cancer cells.

Therefore, it might be suggested that these marine algae-derived NPs have potent capacities for new anticancer product developments in the pharmaceutical as well as the food industries as novel chemopreventing agents for cancer therapy.

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