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cots, papayas etc), vegetables, including carrots, sweet potatoes, arugula, watercress, broccoli, pumpkins, tomatoes as well as less processed carbohydrate rich
staple foods daily could reduce the incidence of cancer by 20 percent (Basu et al.
2001). Additionally, diets that are rich in fruits and vegetables that are rich in carotenoids can reduce the risk, development and continuity of cancer (Rock 2009).
Lutein, zeaxanthin, fucoxanthin, α-carotene, β-carotene, astaxanthin and
β-cryptoxanthin are examples of carotenoids that displayed anticancer activity and
may be essential in the prevention of cancer (Nishino et al. 2002). Due to their useful effects on human health such as stimulation of immune system and inhibition of
cancer cells (which are all linked to their antioxidant role), scientific interest on
carotenoids have increase over the years (Das et al. 2007). Lycopene is the main
carotenoid that exists in the serum and it is reported to stimulate the connexion43
expression, a gene that codes for the gap junction protein that can cause upregulation of gap junction potentially preventing cancer cell proliferation (Zhang et  al.
1991; Zhang et al. 1992; Rao and Agarwal 1999). Moreover, increased consumption
of xanthophyll carotenoids found in human plasma including cryptoxanthin, lutein
and zeaxanthin is reported to decreases the incidence of age-related disorders like
cancer, cataract formation, macular degeneration and cardiovascular disorders
(Bhosale and Bernstein 2005). Fucoxanthin is another interesting carotenoids that is
abundantly found in Undaria pinnatifida (Liu et al. 2009). It was reported that it
causes apoptosis of human HL-60 cancer cell by causing fragmentation of DNA and
inhibition of cell proliferation (Hosokawa et al. 1999). In another in vitro study, it
inhibits the proliferation of murine embryonic liver BNL CL.2 cells and human
hepatoma SK-Hep1 cells (Liu et al. 2009). Fucoxanthin effectively decreases the
motility of cancer cell lines of human colon like DLD-1, HT-29, and Caco2
(Hosokawa et  al. 2004). Additionally, it causes the arrest of cell cycle at G0G1
phase in adenocarcinoma WiDr cells of human colon (Das et al. 2005) and hepatocarcinoma HepG2 cells of humans (Das et al. 2008).
PPARγ is a type of nuclear hormone receptor superfamily and acts as a ligand
activated transcription factor. It is involved in several pathological and physiological processes, like lipid metabolism, insulin sensitivity, lipid metabolism and growth
of cells in different organs and occurrence of many human disorders including dyslipidaemia, cancer, inflammation, obesity and atherosclerosis (Lehrke and Lazar
2005; Feige et al. 2006; Semple et al. 2006). Also, PPARγ ligands synthesized in the
body include linolenic acid, arachidonic acid and linoleic acid as well as 15-deoxy∆
12,14
-prostaglandin J 2 (15d-PGJ 2 ). Synthetic PPARγ ligands include the glizers also
called known as the thiazolidinediones (rosiglitazone, ciglitazone, troglitazone and
pioglitazone), which are ususally used in the treatment of type-2 diabetes. The
ligands of the PPARγ (also called PPARγ agonists) forms a heterodimer with the
RXR-α and react with its major response elements, PPREs, situated in the promoter
region of the different target genes (Zhao et al. 2016). Emerging reports indicated
that PPARγ is expressed in several tissues in human which includes the colon, stomach, breast, thyroid, lung, prostate and ovary, where it controls cell differentiation,
proliferation and apoptosis. This feature makes PPARγ a vital target protein for the
manufacture of new and efficacious anticancer drugs (Han and Roman 2007; Ondrey
A. Olatunde et al.
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