Suppression of Human Pancreatic Carcinoma Cell Growth and Invasion by Epigallocatechin-3-Gallate

Takada, Moriatsu; Nakamura, Yoichiro; Koizumi, Ttamio; Toyama, Hirochika; Kamigaki, Takashi; Suzuki, Yasuyuki; Takeyama, Yoshifumi; Kuroda, Yoshikazu

doi:10.1097/00006676-200207000-00012

Cited by 61 publications

(44 citation statements)

References 19 publications

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“…Most cell culture (20)(21)(22)(23)38) and animal studies (24,25,39) in pancreatic cancer models support our results that high dietary intake of flavonols and flavan-3-ols might inhibit human pancreatic carcinogenesis. The exception is one Argentinean research group, which showed that dietary quercetin increases the incidence of pancreatic dysplastic foci in rats treated with the carcinogen nitrosomethylurea (40,41).…”

Section: Discussionsupporting

confidence: 74%

“…Parsley, thyme, and celery are the primary dietary sources of the two major flavones apigenin and luteolin. Based on the protective effect of flavonoids against pancreatic carcinogenesis in most cell culture (20)(21)(22)(23) and animal studies (24,25), we hypothesized that high dietary intake of flavonols, flavan-3-ols, and flavones may inhibit development of exocrine pancreatic cancer in humans. The association between flavonoid intake and pancreatic cancer development has been evaluated in three prospective cohorts.…”

Section: Introductionmentioning

confidence: 99%

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Flavonoid Intake and Risk of Pancreatic Cancer in Male Smokers (Finland)

Bobe

Weinstein²,

Albanês³

et al. 2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Extending research on the protective effect of flavonoids in cell culture and animal studies, we examined the association between consumption of flavonoids and flavonoid-rich foods and development of exocrine pancreatic cancer within the A-Tocopherol, B-Carotene Cancer Prevention Study cohort. Of the 27,111 healthy male smokers (50-69 years) who completed a selfadministered dietary questionnaire at baseline, 306 developed exocrine pancreatic cancer during follow-up (1985-2004; median, 16.1 years). Intakes of total flavonoids, three flavonoid subgroups, seven individual flavonoids, and flavonoid-rich foods were estimated from a validated food frequency questionnaire. Hazard ratios and 95% confidence intervals were estimated using Cox proportional hazards models. Overall, flavonoid intake was not significantly associated with pancreatic cancer. However, in stratified analysis, greater total flavonoid intake was associated with decreased pancreatic cancer risk in participants randomized during the trial to placebo (fourth versus first quartile: hazard ratio, 0.36; 95% confidence interval, 0.17-0.78; P trend = 0.009) and not to supplemental A-tocopherol (50 mg/d) and/or B-carotene (20 mg/d; P interaction = 0.002). Similar patterns and significant interactions were observed for flavonols, flavan-3-ols, kaempferol, quercetin, catechin, and epicatechin. Our data suggest that a flavonoid-rich diet may decrease pancreatic cancer risk in male smokers not consuming supplemental A-tocopherol and/or B-carotene. (Cancer Epidemiol Biomarkers Prev 2008;17(3):553-62)

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Section: Discussionsupporting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Flavonoid Intake and Risk of Pancreatic Cancer in Male Smokers (Finland)

Bobe

Weinstein²,

Albanês³

et al. 2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…EGCG also selectively inhibits COX-2 without affecting COX-1 expression (Hussain et al, 2005) and down-regulates K-ras (Lyn-Cook et al, 1999), suggesting its effects on the inactivation of oncogenes. Furthermore, the treatment of PANC1, Mia-PaCa-2, and BxPC-3 pancreatic cell lines with EGCG caused significant suppression of the invasive ability of the pancreatic cancer cells (Takada et al, 2002). These reports provide strong evidence in support of the roles of EGCG in chemoprevention and/or treatment of pancreatic cancer, especially because EGCG targets important cell signaling molecules as depicted in Figure 1.…”

Section: Egcgmentioning

confidence: 71%

Pancreatic cancer: Pathogenesis, prevention and treatment

Sarkar

Banerjee

2007

Toxicology and Applied Pharmacology

104

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Pancreatic cancer is the fourth leading cause of cancer death in the United States with a very low survival rate of 5 years. To better design new preventive and/or therapeutic strategies for the fight against pancreatic cancer, the knowledge of the pathogenesis of pancreatic cancer at the molecular level is very important. It has been known that the development and the progression of pancreatic cancer are caused by the activation of oncogenes, the inactivation of tumor suppressor genes, and the deregulation of many signaling pathways among which the EGFR, Akt, and NF-κB pathways appear to be most relevant. Therefore, the strategies targeting EGFR, Akt, NF-κB, and their downstream signaling could be promising for the prevention and/or treatment of pancreatic cancer. In this brief review, we will summarize the current knowledge regarding the pathogenesis, prevention, and treatment of pancreatic cancer.

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“…Perhaps most notably, the anticancer properties of green tea flavanols have been reported in animal models and in human cell lines , as well as in human intervention studies [60]. On the other hand, green tea consumption has been proposed as significantly reducing the risk of cancer of the biliary tract [133], bladder [110], breast [74], and colon [72]. Many of the anti-cancer properties associated with green tea are thought to be mediated by the flavanol Epigallocatechin gallate (EGCG), which has been shown to induce apoptosis and inhibit cancer cell growth by altering the expression of cell cycle regulatory proteins and the activity of signaling proteins involved in cell proliferation, transformation, and metastasis [66].…”

Section: Antioxidants In Cancer Assaysmentioning

confidence: 99%