Fish oil ingestion reduces the number of aberrant crypt foci and adenoma in 1,2-dimethylhydrazine-induced colon cancer in rats

Moreira, António Paulo; Sabarense, Céphora Maria; Dias, Camila Carneiro; Lunz, Wellington; Natali, Antônio José; Glória, Maria Beatriz Abreu; Peluzio, M.C.G.

doi:10.1590/s0100-879x2009007500015

Cited by 12 publications

(3 citation statements)

References 22 publications

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“…Given that results are rather consistent when fish intake is considered ( 4 ) , one could expect comparable observations, serum LC-ω 3PUFA being highly correlated with fish intake ( 14 , 21 ) . Several experimental studies support the hypothesis of CRC risk reduction by LC ω3 PUFA ( 22 – 25 ) through different mechanisms In addition, the hypothesis of the anti-inflammatory effect of LC-ω3PUFA and especially EPA ( 26 ) is supported by the subgroup study nested in the PHS, based on biomarkers ( 13 ) , showing a significant interaction with the absence of aspirin treatment (Table 2). However, epidemiological studies are as yet inconsistent, revealing the difficulty of studies focusing on one specific type of nutrient within the context of a multifactorial disease and subjected to confounding and imprecision of exposure measurement.…”

Section: Colorectal Cancermentioning

confidence: 82%

Omega-3 fatty acids and cancers: a systematic update review of epidemiological studies

Gerber¹

2012

Br J Nutr

177

108

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Experimental models showed consistently a modulation of carcinogenesis by omega 3 polyunsaturated fatty acids (v3 PUFA). Fish intake is often described as part of a beneficial dietary pattern. However, observational epidemiological studies on the relationship between v3 PUFA reported conflicting results. The objective of this systematic review is to determine whether there exists any progress in the evaluation of the causal relationship between dietary v3 PUFA and cancers since the previous FAO/OMS expert consultation and whether it is possible to propose preventive and/or adjuvant therapeutic recommendations. Prospective and case-control observational studies published since 2007 and meeting validity criteria were considered together with RCT. Experimental studies are mentioned to provide for biological plausibility. When evaluating the level of evidence, a portfolio approach was used, weighted by a hierarchy giving higher importance to prospective studies followed by RCT if any. There is a probable level of evidence that ALA per se is neither a risk factor nor a beneficial factor with regards to cancers. Observational studies on colorectal, prostate and breast cancers only provided limited evidence suggesting a possible role of LC-v3PUFA in cancer prevention because insufficient homogeneity of the observations. Explanation for heterogeneity might be the inherent difficulties associated with epidemiology (confounding and dietary pattern context, measurement error, level of intake, genetic polymorphism). The role of LC-v3PUFA as adjuvant, might be considered of possible use, in view of the latest RCT on lung cancers even if RCT on other cancers still need to be undertaken.Key words: Omega 3 fatty acids: EPA: DHA: alpha linolenic acid: cancers: epidemiologic studies Rationale: The incidence of cancers affected almost 13 million people and caused more than 7 million deaths worldwide in 2008. Incidence is expected to increase to 15 million in 2015 and death to more than 9 million due to demographic effects alone. However increased longevity is not the only explanation, e.g. in France the incidence of cancers in males increased by 35 % and in females by 43 % after controlling for the demographic effect (1) Thus it is generally acknowledged that changes in exposure to carcinogenic environment and in nutrition are factors of this evolution.If changes in food patterns are more often associated with an increased incidence of cancers, as illustrated in migrant studies (2) , it happens that nutritional recommendations are followed by a decreased incidence (3) . This underlines the search for beneficial nutrients. Several epidemiological studies have shown a risk reduction of some cancers associated with long chain omega3 fatty acids (v3 LC-PUFA) or fish intake (4) , but the limited evidence or the absence of consistency required further investigations.A systematic review of the epidemiological studies published since 2007 is undertaken here focusing on v3 LC-PUFA either from dietary intake (but not considering fis...

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Section: Colorectal Cancermentioning

confidence: 82%

Omega-3 fatty acids and cancers: a systematic update review of epidemiological studies

Gerber¹

2012

Br J Nutr

177

108

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“…The omega-3 polyunsaturated fatty acids (n-3 PUFAs) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) induce degradation of EZH2 through a posttranslational mechanism via a proteasome-mediated pathway [21]. A fish oil diet rich in n-3 PUFAs reduced colonic polyps and adenomas in dimethylhydrazineinduced colon cancer in rats, was associated with lower risk of breast cancer, and a significant 63% reduction in prostate cancer-specific mortality [22][23][24]. Thus, modulation of HMTs for prevention can be potentially achieved with drug, small molecule, or dietary intervention.…”

Section: Introductionmentioning

confidence: 99%

Chromatin remodeling by the histone methyltransferase EZH2 drives lung pre-malignancy and is a target for cancer prevention

et al. 2021

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Background Trimethylation of lysine 27 and dimethylation of lysine 9 of histone-H3 catalyzed by the histone methyltransferases EZH2 and G9a impede gene transcription in cancer. Our human bronchial epithelial (HBEC) pre-malignancy model studied the role of these histone modifications in transformation. Tobacco carcinogen transformed HBEC lines were characterized for cytosine DNA methylation, transcriptome reprogramming, and the effect of inhibiting EZH2 and G9a on the transformed phenotype. The effects of targeting EZH2 and G9a on lung cancer prevention was assessed in the A/J mouse lung tumor model. Results Carcinogen exposure induced transformation and DNA methylation of 12–96 genes in the four HBEC transformed (T) lines that was perpetuated in malignant tumors. In contrast, 506 unmethylated genes showed reduced expression in one or more HBECTs with many becoming methylated in tumors. ChIP-on-chip for HBEC2T identified 327 and 143 genes enriched for H3K27me3 and H3K9me2. Treatment of HBEC2T and HBEC13T with DZNep, a lysine methyltransferase inhibitor depleted EZH2, reversed transformation, and induced transcriptional reprogramming. The EZH2 small molecule inhibitor EPZ6438 also affected transformation and expression in HBEC2T, while a G9a inhibitor, UNC0642 was ineffective. Genetic knock down of EZH2 dramatically reduced carcinogen-induced transformation of HBEC2. Only DZNep treatment prevented progression of hyperplasia to adenomas in the NNK mouse lung tumor model through reducing EZH2 and affecting the expression of genes regulating cell growth and invasion. Conclusion These studies demonstrate a critical role for EZH2 catalyzed histone modifications for premalignancy and its potential as a target for chemoprevention of lung carcinogenesis.

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“…Fish oil is a substance containing poly-unsaturated fatty acid (PUFA) such as ω-3-eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which play a role in inducing cellular apoptosis and differentiation, as well as inhibiting cell proliferation. Accumulation of ω-3 PUFAs on the cell membrane are predicted to maintain the fluidity, receptor binding to its ligand, determine the activity of the enzymes such as ornithine decarboxylase (ODC), and transduction pathways (Moreira et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Inhibition Activities of Fish Oil in iNOs, COX-2, and β-Catenin Expressions in Colorectal Preneoplasia of Mice Induced by Azoxymetane and Dextran Sodium Sulfate

Priosoeryanto¹,

Harlina²,

Cornain³

2014

Journal of Applied Biotechnology

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Epidemiological studies of the relationship between dietary fish oil and risk of colorectal cancer have been inconsistent. The present study was conducted in order to determine the ISSN 2327-0640 2014 www.macrothink.org/jab 92 inhibitory effect of fish oil on inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, and β-catenin expressions in the colorectal preneoplasia development of mice induced by azoxymetane (AOM) and dextran sodium sulfate (DSS). In this study, balb/c mice was injected intraperitoneally by a single dose of 10 mg/kg of body weight AOM followed by administered of 1% DSS during a week in drinking water. Fish oil was administered orally in three different doses (1.5 mg/ low dose, 3 mg/ medium dose and 6 mg/high dose) in each group of mice per day until the mice were terminated. The expression of iNOs, COX-2, and β-catenin were observed in the epithelial cells of colon mucosa crypts. In the second month, the iNOs expression was decreased in the medium and high groups of fish oil. In the third and fourth month, decreasing of the iNOs expression were observed in all groups (p<0.05). The COX-2 expression was decreased in the medium and high groups on the second month. The expression of β-catenin was also decreased in the medium group on the fourth month. The inhibition effect of high dose of fish oil on β-catenin was observed on the third month. In conclusion, administration of medium dose of fish oil in mice induced by AOM/DSS was the most effective dose to decreased the expression of iNOs, COX-2, and β-catenin in the second month. Journal of Applied Biotechnology

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Fish oil ingestion reduces the number of aberrant crypt foci and adenoma in 1,2-dimethylhydrazine-induced colon cancer in rats

Cited by 12 publications

References 22 publications

Omega-3 fatty acids and cancers: a systematic update review of epidemiological studies

Omega-3 fatty acids and cancers: a systematic update review of epidemiological studies

Chromatin remodeling by the histone methyltransferase EZH2 drives lung pre-malignancy and is a target for cancer prevention

Inhibition Activities of Fish Oil in iNOs, COX-2, and β-Catenin Expressions in Colorectal Preneoplasia of Mice Induced by Azoxymetane and Dextran Sodium Sulfate

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