Effect of selenium-enriched malt on VEGF and several relevant angiogenic cytokines in diethylnitrosamine-induced hepatocarcinoma rats

Liu, Jiaguo; Zhao, Haizhen; Liu, Yanjuan; Wang, Xiaolong

doi:10.1016/j.jtemb.2009.10.001

Cited by 15 publications

(15 citation statements)

References 39 publications

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“…For example, in an orthotopic model of human colon cancer in athymic nude mice, selenium supplementation with methylselenocysteine resulted in significant inhibition of microvessel formation and tumor growth [61]. Other studies have also demonstrated similar anti-angiogenic effects of organic selenium supplements in cancer cells and tissues [62,63]. Similar results have also been observed in non-tumorigenic tissues.…”

Section: Biphasic Effects Of Selenium Statusmentioning

confidence: 72%

Selenistasis: Epistatic Effects of Selenium on Cardiovascular Phenotype

Joseph

Loscalzo

2013

Nutrients

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Although selenium metabolism is intricately linked to cardiovascular biology and function, and deficiency of selenium is associated with cardiac pathology, utilization of selenium in the prevention and treatment of cardiovascular disease remains an elusive goal. From a reductionist standpoint, the major function of selenium in vivo is antioxidant defense via its incorporation as selenocysteine into enzyme families such as glutathione peroxidases and thioredoxin reductases. In addition, selenium compounds are heterogeneous and have complex metabolic fates resulting in effects that are not entirely dependent on selenoprotein expression. This complex biology of selenium in vivo may underlie the fact that beneficial effects of selenium supplementation demonstrated in preclinical studies using models of oxidant stress-induced cardiovascular dysfunction, such as ischemia-reperfusion injury and myocardial infarction, have not been consistently observed in clinical trials. In fact, recent studies have yielded data that suggest that unselective supplementation of selenium may, indeed, be harmful. Interesting biologic actions of selenium are its simultaneous effects on redox balance and methylation status, a combination that may influence gene expression. These combined actions may explain some of the biphasic effects seen with low and high doses of selenium, the potentially harmful effects seen in normal individuals, and the beneficial effects noted in preclinical studies of disease. Given the complexity of selenium biology, systems biology approaches may be necessary to reach the goal of optimization of selenium status to promote health and prevent disease.

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Section: Biphasic Effects Of Selenium Statusmentioning

confidence: 72%

Selenistasis: Epistatic Effects of Selenium on Cardiovascular Phenotype

Joseph

Loscalzo

2013

Nutrients

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“…It was hypothesized that the increase of TXR1 promotes tumor aggressiveness and contributes to poor prognosis, suggesting that optimal redox status could play a prominent role in modulating tumorigenesis. In a carcinogen-induced hepatocarcinoma rat model, Se-enriched malt was found to inhibit angiogenesis at least partially through reducing several angiogenic factors, including TNFα, nitric oxide, nitric oxide synthase, IGF II, VEGF, and protein kinase Cα [52,74]. Selenite supplementation produced a smaller effect, which may have been the result of insufficient reduction of angiogenic factors.…”

Section: Other Cancersmentioning

confidence: 99%

Is Selenium a Potential Treatment for Cancer Metastasis?

2013

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Selenium (Se) is an essential micronutrient that functions as a redox gatekeeper through its incorporation into proteins to alleviate oxidative stress in cells. Although the epidemiological data are somewhat controversial, the results of many studies suggest that inorganic and organic forms of Se negatively affect cancer progression, and that several selenoproteins, such as GPXs, also play important roles in tumor development. Recently, a few scientists have examined the relationship between Se and metastasis, a late event in cancer progression, and have evaluated the potential of Se as an anti-angiogenesis or anti-metastasis agent. In this review, we present the current knowledge about Se compounds and selenoproteins, and their effects on the development of metastasis, with an emphasis on cell migration, invasion, and angiogenesis. In the cancers of breast, prostate, colorectal, fibrosarcoma, melanoma, liver, lung, oral squamous cell carcinoma, and brain glioma, there is either clinical evidence linking selenoproteins, such as thioredoxin reductase-1 to lymph node metastasis; in vitro studies indicating that Se compounds and selenoproteins inhibited cell motility, migration, and invasion, and reduced angiogenic factors in some of these cancer cells; or animal studies showing that Se supplementation resulted in reduced microvessel density and metastasis. Together, these data support the notion that Se may be an anti-metastastatic element in addition to being a cancer preventative agent.

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“…The source of these disparities remains unclear but may be caused by physiologic deference associated with ethnicity, including cytochrome P450 3A4 (CYP3A4) and uridine diphosphate glucuronosyltransferase 1A9 (UGT1A9) 8, 9. Also, it has been suggested that VEGF and tumor necrosis factor‐α (TNF‐α) are overexpressed in patients with HCC, and the VEGF pathway is important in the causation of HFSR 8, 10‐13. Thus, further investigations on the genetic association between sorafenib‐induced HFSR and single nucleotide polymorphisms (SNPs) of VEGF , TNF ‐α, CYP3A4 , and UGT1A9 are warranted to determine the risk of sorafenib‐induced HFSR.…”

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confidence: 99%

Genetic predisposition of hand‐foot skin reaction after sorafenib therapy in patients with hepatocellular carcinoma

Lee

Chung

Kim

et al. 2012

Cancer

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BACKGROUND: Sorafenib currently sets the new standard for advanced hepatocellular carcinoma (HCC). It has been suggested that Asian patients with HCC have increased susceptibility to hand‐foot skin reaction (HFSR) related to sorafenib therapy. The authors investigated the association between sorafenib‐induced HFSR and genetic polymorphisms in Korean patients with HCC. METHODS: For this prospective cohort study, the authors enrolled 59 consecutive patients with intermediate stage HCC from 5 centers in Korea. All patients received sorafenib 400 mg twice daily in combination with transarterial chemoembolization (TACE). Genotyping was performed on a total of 49 single nucleotide polymorphisms (SNPs) in 8 candidate genes (minor allelic frequency ≥5%). Serum levels of vascular endothelial growth factor (VEGF) and tumor necrosis factor‐alpha (TNF‐α) were measured using enzyme‐linked immunosorbent assays before therapy and 1 month after therapy. RESULTS: During a median treatment period of 18 months, 55 patients (93%) developed sorafenib‐induced HFSR, including grade 1 reactions in 15 patients, grade 2 reactions in 27 patients, and grade 3 reaction in 13 patients. The SNPs TNF‐α −308GG, VEGF −94GG, VEGF 1991CC, VEGF IVS3‐28CC, and uridine diphosphate glucuronosyltransferase 1 family‐polypeptide A9 (UGT1A9) IVS1‐37431AA were associated significantly with the development of high‐grade (grade 2 or 3) HFSR in univariate analysis (P < .05). In multivariate analysis, the SNPs VEGF 1991CC (odds ratio, 45.7), TNF‐α −308GG (odds ratio, 44.1), and UGT1A9 IVS1‐37431AA (odds ratio, 18.7) were identified as independent risk factors for the development of high‐grade HFSR (P = .01, P = .02, and P = .02, respectively). He serum TNF‐α level measured 1 month after sorafenib therapy was correlated significantly with the development of high‐grade HFSR (odds ratio, 3.56; P = .026). CONCLUSIONS: Differences in the incidence of HFSR may have been caused by ethnic differences in genetic polymorphisms of the TNF‐α, VEGF, and UGT1A9 genes, especially in relation to the expression of serum TNF‐α after sorafenib therapy. Cancer 2013. © 2012 American Cancer Society.

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Effect of selenium-enriched malt on VEGF and several relevant angiogenic cytokines in diethylnitrosamine-induced hepatocarcinoma rats

Cited by 15 publications

References 39 publications

Selenistasis: Epistatic Effects of Selenium on Cardiovascular Phenotype

Selenistasis: Epistatic Effects of Selenium on Cardiovascular Phenotype

Is Selenium a Potential Treatment for Cancer Metastasis?

Genetic predisposition of hand‐foot skin reaction after sorafenib therapy in patients with hepatocellular carcinoma

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