by modulating protein expression in HT-29 cells. FNDF inhibited HT-29 cell
growth and modulated protein expression associated with apoptosis, cell cycle
arrest, and proliferation, as well as morphological changes linked to apoptosis
evaluated by TUNEL and hematoxylin and eosin stains, confirming previous
results on gene expression.
Diet that inhibits one or more neoplastic events and reduces cancer risk has
been suggested as a preventive approach to control breast cancer. Ray et al. (2010)
used human breast cancer cells and primary human mammary epithelial cells as an
in vitro model to assess the efficacy of Bitter Melon (Momordica charantia)
Extract (BME) as an anticancer agent. The BME treatment enhanced p53, p21, and
pChk1/2 and inhibited cyclin B1 and cyclin D1 protein expressions, suggesting a
mechanism involving cell cycle regulation. Sesamin, a lipid-soluble lignan, a class
of phytoestrogen, isolated from sesame (Sesamum indicum), inhibited the proliferation of a wide variety of tumor cells including leukemia, multiple myeloma, and
cancers of the colon, prostate, breast, pancreas, and lung (Harikumar et al. 2010).
In this study, sesamin also potentiated tumor necrosis factor-a–induced apoptosis
and this correlated with the suppression of gene products linked to cell survival,
proliferation, inflammation, invasion, and angiogenesis. Sesamin down-regulated
constitutive and inducible NF-jB activation induced by various inflammatory
stimuli and carcinogens, and inhibited the degradation of IjBa, thereby indicating
its potential against cancer and other chronic diseases through the suppression of
NF-jB signaling pathway. Dark chocolate protects against colon cancer by
inhibiting Aberrant Crypt Foci (ACF) formation by down-regulating cyclooxygenase 2 and RelA (inflammatory mediators) gene expression (DeIulio and Hong
2010); whereas blueberry phytochemicals inhibit growth and metastatic potential
of MDA-MB-231 breast cancer cells through modulation of the phosphatidylinositol 3-kinase pathway (Adams et al. 2010). Intake of grape-derived polyphenols
effectively reduced the development of colon carcinoma tumors in vivo by
blunting tumor vascularization and by inhibiting proliferation and promoting
apoptosis of tumor cells subsequent to an upregulation of tumor suppressor genes
(Walter et al. 2010).
The above observations may indicate that whole food products rather than
single bioactive components are important in mediating physiological effects in the
body. However, other studies support the idea ‘‘of a single compound.’’ For
example, Caffeic Acid Phenethyl Ester (CAPE, a phenolic compound) in a single
dose administered before carcinogenic initiation induced by Diethylnitrosamine
(DEN) prevents the appearance of preneoplastic lesions of hepatocarcinogenesis
initiation (Beltrán-Ramírez et al. 2010). Comparison of gene expression profiles
induced by DEN with a previously administered single dose of CAPE showed that
DEN treatment increased gene expression associated with oxidative stress, genes
cell cycle regulation, and cytochrome P450 modification. CAPE plus DEN
reduced the expression of cytochrome involved in DEN bioactivation as well as
the expression of oxidative stress and cell cycle regulators. In other study, dietary
omega-3 (n-3) Polyunsaturated Fatty Acids (PUFA) suppressed expression of
294
R. Campos-Vega et al.
growth and modulated protein expression associated with apoptosis, cell cycle
arrest, and proliferation, as well as morphological changes linked to apoptosis
evaluated by TUNEL and hematoxylin and eosin stains, confirming previous
results on gene expression.
Diet that inhibits one or more neoplastic events and reduces cancer risk has
been suggested as a preventive approach to control breast cancer. Ray et al. (2010)
used human breast cancer cells and primary human mammary epithelial cells as an
in vitro model to assess the efficacy of Bitter Melon (Momordica charantia)
Extract (BME) as an anticancer agent. The BME treatment enhanced p53, p21, and
pChk1/2 and inhibited cyclin B1 and cyclin D1 protein expressions, suggesting a
mechanism involving cell cycle regulation. Sesamin, a lipid-soluble lignan, a class
of phytoestrogen, isolated from sesame (Sesamum indicum), inhibited the proliferation of a wide variety of tumor cells including leukemia, multiple myeloma, and
cancers of the colon, prostate, breast, pancreas, and lung (Harikumar et al. 2010).
In this study, sesamin also potentiated tumor necrosis factor-a–induced apoptosis
and this correlated with the suppression of gene products linked to cell survival,
proliferation, inflammation, invasion, and angiogenesis. Sesamin down-regulated
constitutive and inducible NF-jB activation induced by various inflammatory
stimuli and carcinogens, and inhibited the degradation of IjBa, thereby indicating
its potential against cancer and other chronic diseases through the suppression of
NF-jB signaling pathway. Dark chocolate protects against colon cancer by
inhibiting Aberrant Crypt Foci (ACF) formation by down-regulating cyclooxygenase 2 and RelA (inflammatory mediators) gene expression (DeIulio and Hong
2010); whereas blueberry phytochemicals inhibit growth and metastatic potential
of MDA-MB-231 breast cancer cells through modulation of the phosphatidylinositol 3-kinase pathway (Adams et al. 2010). Intake of grape-derived polyphenols
effectively reduced the development of colon carcinoma tumors in vivo by
blunting tumor vascularization and by inhibiting proliferation and promoting
apoptosis of tumor cells subsequent to an upregulation of tumor suppressor genes
(Walter et al. 2010).
The above observations may indicate that whole food products rather than
single bioactive components are important in mediating physiological effects in the
body. However, other studies support the idea ‘‘of a single compound.’’ For
example, Caffeic Acid Phenethyl Ester (CAPE, a phenolic compound) in a single
dose administered before carcinogenic initiation induced by Diethylnitrosamine
(DEN) prevents the appearance of preneoplastic lesions of hepatocarcinogenesis
initiation (Beltrán-Ramírez et al. 2010). Comparison of gene expression profiles
induced by DEN with a previously administered single dose of CAPE showed that
DEN treatment increased gene expression associated with oxidative stress, genes
cell cycle regulation, and cytochrome P450 modification. CAPE plus DEN
reduced the expression of cytochrome involved in DEN bioactivation as well as
the expression of oxidative stress and cell cycle regulators. In other study, dietary
omega-3 (n-3) Polyunsaturated Fatty Acids (PUFA) suppressed expression of
294
R. Campos-Vega et al.