Alterations of pRb1-cyclin D1-cdk4/6-p16INK4A pathway in endometrial carcinogenesis

Semczuk, Andrzej; Jakowicki, J

doi:10.1016/j.canlet.2003.09.012

“…46 Recent studies have shown that polyphenols can inhibit different cells at different cell phases: G1, S, S/G2, and G2 47 (see also Fig. 2).…”

Section: F Cell Cycle Arrest and Induction Of Apoptosismentioning

confidence: 94%

“…EGCG has been shown to directly inhibit CDKs, 48 or indirectly by inducing the expression of p21 and p27 genes and inhibiting the expression of cyclin d1 and Rb phosphorylation. 46,48,49 Resveratrol was shown to arrest HL-60 cells at the S/G2-phase transition and subsequently increase the cell number in the G1/S phases, due to an overexpression of cyclins A and E without modification of p21 expression. 50 In addition it has been found that caffeic acid phenethyl ester (CAPE , Table I) is also able to cause growth arrest in human leukemia HL-60 cells.…”

Section: F Cell Cycle Arrest and Induction Of Apoptosismentioning

confidence: 99%

New insights on the anticancer properties of dietary polyphenols

Fresco

¹

,

Borges

²

,

Diniz

³

et al. 2006

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Cancer, one of the major causes of death across the world, has shown to be a largely preventable disease, highly susceptible to modulation by dietary factors. Phenolic compounds, abundant in vegetables and fruits ubiquitous in diet, were described to play an important role as chemopreventive agents. Since conventional therapeutic and surgical approaches have not been able to control the incidence of most cancer types, the development of chemopreventive strategies is an urgent priority in public health. The current diet phenolic intake is often insufficient to protect from mutagens (either exogenous or endogenous), which leads to the need for dietary supplementation as an alternative approach. Research efforts are placing increasing emphasis on identifying the biological mechanisms and in particular the signal transduction pathways related to the chemopreventive activities of these compounds. These effects are believed to occur by the regulation of signaling pathways such as nuclear factor-kB (NF-kB), activator protein-1 (AP-1) or mitogen-activated protein kinases (MAPK). Dietary polyphenols can exert their effects on these pathways separately or sequentially and in addition the occurrence of crosstalk between these pathways cannot be overlooked. By modulating cell signaling pathways, polyphenols activate cell death signals and induce apoptosis in precancerous or malignant cells resulting in the inhibition of cancer development or progression. However, regulation of cell signaling pathways by dietary polyphenols can also lead to cell proliferation/survival or inflammatory responses due to increased expression of several genes. The present review summarizes the most recent advances providing new insights into the molecular mechanisms underlying the promising anticarcinogenic activity of dietary polyphenols. ß

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“…6). 48,79 HBx increases the rate and level of activation of CDK2, where the rate is associated with cyclins E and A, and the level with cyclin B. 80 HBx also causes cyclin D1 overexpression, 81 the Rb gene is a key player in the G1/S checkpoint system, and HBxAg transactivates the Rb promoter.…”

Section: Ink4dmentioning

confidence: 99%

Molecular Pathogenesis of Hepatitis-B-virus-associated Hepatocellular Carcinoma

Park¹,

Song²,

Chung³

2007

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Hepatocellular carcinoma (HCC) is one of the most frequent and malignant diseases worldwide. Epidemiological studies have clearly demonstrated that chronic hepatitis B virus (HBV) infection is a major etiological factor in the development of HCC. The pathogenesis of HBV-associated HCC has been studied extensively, and the molecular changes associated with malignant transformation have been identified. The predominant carcinogenic mechanisms of HBV-associated HCC are chronic inflammation and the effects of cytokines in the development of fibrosis and liver cell proliferation. An important role is also played by the integration of HBV DNA into host cellular DNA, which disrupts or promotes the expression of cellular genes that are important in cell growth and differentiation. Especially, HBx protein is a transactivating protein that promotes cell growth, survival, and the development of HCC. Continued investigation of the mechanisms underlying hepatocarcinogenesis will refine our current understanding of the molecular and cellular basis for neoplastic transformation in the liver. Prevention of HBV infections and effective treatments for chronic hepatitis B are still needed for the global control of HBV-associated HCC. This review summarizes the current knowledge on the mechanisms involved in HBV-associated hepatocarcinogenesis. (Gut and Liver 2007;1: 101-117)

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“…46 Recent studies have shown that polyphenols can inhibit different cells at different cell phases: G1, S, S/G2, and G2…”

Section: F Cell Cycle Arrest and Induction Of Apoptosismentioning

confidence: 99%

New Insights on the Anticancer Properties of Dietary Polyphenols

Fresco

¹

,

Borges

²

,

Diniz

³

et al. 2007

View full text Add to dashboard Cite

Cancer, one of the major causes of death across the world, has shown to be a largely preventable disease, highly susceptible to modulation by dietary factors. Phenolic compounds, abundant in vegetables and fruits ubiquitous in diet, were described to play an important role as chemopreventive agents. Since conventional therapeutic and surgical approaches have not been able to control the incidence of most cancer types, the development of chemopreventive strategies is an urgent priority in public health. The current diet phenolic intake is often insufficient to protect from mutagens (either exogenous or endogenous), which leads to the need for dietary supplementation as an alternative approach. Research efforts are placing increasing emphasis on identifying the biological mechanisms and in particular the signal transduction pathways related to the chemopreventive activities of these compounds. These effects are believed to occur by the regulation of signaling pathways such as nuclear factor-kB (NF-kB), activator protein-1 (AP-1) or mitogen-activated protein kinases (MAPK). Dietary polyphenols can exert their effects on these pathways separately or sequentially and in addition the occurrence of crosstalk between these pathways cannot be overlooked. By modulating cell signaling pathways, polyphenols activate cell death signals and induce apoptosis in precancerous or malignant cells resulting in the inhibition of cancer development or progression. However, regulation of cell signaling pathways by dietary polyphenols can also lead to cell proliferation/survival or inflammatory responses due to increased expression of several genes. The present review summarizes the most recent advances providing new insights into the molecular mechanisms underlying the promising anticarcinogenic activity of dietary polyphenols. ß

show abstract

Alterations of pRb1-cyclin D1-cdk4/6-p16INK4A pathway in endometrial carcinogenesis

Cited by 86 publications

References 80 publications

New insights on the anticancer properties of dietary polyphenols

New insights on the anticancer properties of dietary polyphenols

Molecular Pathogenesis of Hepatitis-B-virus-associated Hepatocellular Carcinoma

New Insights on the Anticancer Properties of Dietary Polyphenols

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