Dietary Flavonoid and Cancer Prevention: Evidence and Potential Mechanism

Kuo, Shiu‐Ming

doi:10.1615/critrevoncog.v8.i1.30

Cited by 147 publications

(103 citation statements)

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“…In contrast to the high incidence of prostate cancer in North America, the incidence of this disease in East Asia is very low [7,8]. The low incidence of prostate cancer in Asian men has been attributed to the dietary consumption of large amounts of plant-based foods rich in phytochemicals [9][10][11]. Because of these observations, nutritional supplements such as soybean, garlic, and green tea, which are rich in polyphenolic compounds, have been used to augment anticancer therapies [12,13].…”

Section: Introductionmentioning

confidence: 99%

Role of p53, PUMA, and Bax in wogonin-induced apoptosis in human cancer cells

Lee

Kim

Zhang

et al. 2008

Biochemical Pharmacology

120

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We observed that treatment of prostate cancer cells for 24 h with wogonin, a naturally occurring monoflavonoid, induced cell death in a dose-and time-dependent manner. Exposure of wogonin to LNCaP cells was associated with increased intracellular levels of p21 Cip-1 , p27 Kip-1 , p53, and PUMA, oligomerization of Bax, release of cytochrome c from the mitochondria, and activation of caspases. We also confirmed the role of p53 by noting that knock-in in p53 expression by transfecting p53 DNA increased wogonin-induced apoptosis in p53-null PC-3 cells. To study the mechanism of PUMA upregulation, we determined the activities of PUMA promoter in the wogonin treated and untreated cells. Increase of the intracellular levels of PUMA protein was due to increase in transcriptional activity. Data from chromatin immunoprecipitation (ChIP) analyses revealed that wogonin activated the transcription factor p53 binding activity to the PUMA promoter region. We observed that the upregulation of PUMA mediated wogonin cytotoxicity. Further characterization of the transcriptional response to wogonin in HCT116 human colon cancer cells demonstrated that PUMA induction was p53-dependent; deficiency in either p53 or PUMA significantly protected HCT116 cells against wogonin-induced apoptosis. Also, wogonin promoted mitochondrial translocation and multimerization of Bax. Interestingly, wogonin (100 μM) treatment did not affect the viability of normal human prostate epithelial cells (PrEC). Taken together, these results indicate that p53-dependent transcriptional induction of PUMA and oligomerization of Bax play important roles in the sensitivity of cancer cells to apoptosis induced by caspase activation through wogonin.

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Section: Introductionmentioning

confidence: 99%

Role of p53, PUMA, and Bax in wogonin-induced apoptosis in human cancer cells

Lee

Kim

Zhang

et al. 2008

Biochemical Pharmacology

120

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“…The two major classes, flavonoids and phenolic acids, exert strong antioxidant effects in vitro (Rice-Evans et al, 1996) and can elevate the plasma antioxidant capacity in humans in vivo (Whitehead et al, 1995;Serafini et al, 1996;Carbonneau et al, 1997;Day et al, 1997). Several epidemiologic studies suggest protective effects of polyphenols against coronary heart disease ( Hertog, 1996) and cancer (Blot et al, 1996;Kuo, 1997) that might be attributed to their antioxidant properties.…”

Section: Introductionmentioning

confidence: 99%

Plasma antioxidant capacity of HIV-seropositive and healthy subjects during long-term ingestion of fruit juices or a fruit–vegetable-concentrate containing antioxidant polyphenols

et al. 2001

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“…Therefore, dietary flavonoids have attracted attention as chemopreventive agents. 28) Thousands of flavonoids are known to occur in nature, and they are both qualitatively and quantitatively one of the largest groups of natural products. 29) Flavonoids are polyphenolic compounds harboring 15 carbon atoms and two benzene rings joined by a linear three-carbon chain (Fig.…”

Section: Resultsmentioning

confidence: 99%

Induction of Apoptotic Cell Death by Synthetic Naringenin Derivatives in Human Lung Epithelial Carcinoma A549 Cells

Lee

Kang

Choi

et al. 2007

Biological & Pharmaceutical Bulletin

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Lung cancer is one of the most common cancers in many countries and the leading cause of cancer deaths in the world accounting for 28% of all cancer death.1,2) The high mortality of this disease is due to the difficulty of early diagnosis and its high potential to invade locally and metastasize to distant organs. Therefore, there is need for novel diagnosis, treatment, and prevention, against lung cancer.As the functional compounds of the plants can serve as a starting point for the development of optimal derivatives, scientists are always searching for new medical herbs. Flavonoids are plant pigments which have been detected in all parts of plants and major functional components of many herbal preparations used in traditional medical protocols. [3][4][5][6] Fruits and vegetables, as well as popular beverages such as wine, tea, and coffee, are the main dietary sources of flavonoids. It has been reported that flavonoids show pharmacological effects such as antiviral, 7) antitumor, 8) antioxidant, 9,10) and anti-inflammatory activities. 11) They are low molecular weight polyphenolic compounds, which possess a basic 2-phenyl-benzo-gamma-pyrone structure harboring one or more hydroxyl groups. As the result of this basic chemical structure, one of the most obvious features of flavonoids is their ability to quench free radicals via the formation of resonance-stabilized phenoxyl radicals.12) Recently, They have attracted much attention because of their broad pharmacological activities, in particular antioxidant activities, and anti-tumorigenic activities. 13,14) Flavonoids exert protective effects, which appear to be related to specific structural characteristics.15) Recently, several studies have reported that the differential effects of flavonoids are attributable to substituted functional groups. 16,17) We also suggested that the OH group of the -5 or carbon-7 of the C6C3C6 skeleton is the key determinant of the anti-oxidant and anti-apoptotic activities associated with flavonoids.18,19) Therefore, investigations into the structurally related activities of flavonoids are important in terms of our understanding of their differential activities. The association between flavonoid intake and reduced disease risk was originally believed to be the consequence of the anti-oxidant effects of these compounds and recent evidence appears to indicate that flavonoids and their metabolites exert other intracellular effects, including the direct modulation of cell signaling pathways, including the MAPK( Mitogen activated protein kinase) cascade. [20][21][22][23] In this study, we describe the apoptotic cell death of human lung epithelial carcinoma A549 cells as the result of treatment with synthetic naringenin derivates, including 7-Obenzyl naringenin (KUF-1), 7-O-(m-metoxybenzyl) naringenin (KUF-2), 7-O-(2-naphtylmethyl) naringenin (KUF-5), 7-O-benzoxycarbonylmethyl naringenin (KUF-6), 7-O-(MeO-L-Leu-D-Pro-carbonylmethyl) naringenin (KUF-7), and 7-O-(MeO-Gly-D-Pro-carbonylmethyl) naringenin (KUF-8) (Fig. 1). The synthetic naring...

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Dietary Flavonoid and Cancer Prevention: Evidence and Potential Mechanism

Cited by 147 publications

References 0 publications

Role of p53, PUMA, and Bax in wogonin-induced apoptosis in human cancer cells

Role of p53, PUMA, and Bax in wogonin-induced apoptosis in human cancer cells

Plasma antioxidant capacity of HIV-seropositive and healthy subjects during long-term ingestion of fruit juices or a fruit–vegetable-concentrate containing antioxidant polyphenols

Induction of Apoptotic Cell Death by Synthetic Naringenin Derivatives in Human Lung Epithelial Carcinoma A549 Cells

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