Aberrant Epigenetic Alteration in Eca9706 Cells Modulated by Nanoliposomal Quercetin Combined with Butyrate Mediated via Epigenetic-NF-κB Signaling

Naigang, Zheng; Wang, Junling; Yang, Shengli; Wu, Jiahui

doi:10.7314/apjcp.2014.15.11.4539

Cited by 37 publications

(24 citation statements)

References 22 publications

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“…Similar effects have been observed in human Eca9706 esophageal cancer cells using nanoliposomal delivery of quercetin (40 μM), which suppressed cell growth, increased apoptosis, and increased p16INK4α expression (110). Increased p16INK4α expression was associated with decreased p16INK4α gene methylation, as determined by MSP, and decreased expression of DNMT1 (110). …”

Section: Regulation Epigenetic Changessupporting

confidence: 64%

“…Quercetin has also demonstrated DNMT inhibitory effects in human PC3 and DU145 prostate cancer cells, RKO colon cancer cells, and Eca9706 esophageal cancer cells (108–110). The combination of quercetin (12 μM) and curcumin (14 μM) significantly decreased methylation at specific CpG sites within the AR promoter of both PC3 and DU145 prostate cancer cell lines, as determined by sodium bisulfite sequencing (108).…”

Section: Regulation Epigenetic Changesmentioning

confidence: 98%

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Quercetin as an Emerging Anti-Melanoma Agent: A Four-Focus Area Therapeutic Development Strategy

et al. 2016

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Replacing current refractory treatments for melanoma with new prevention and therapeutic approaches is crucial in order to successfully treat this aggressive cancer form. Melanoma develops from neural crest cells, which express tyrosinase – a key enzyme in the pigmentation pathway. The tyrosinase enzyme is highly active in melanoma cells and metabolizes polyphenolic compounds; tyrosinase expression thus makes feasible a target for polyphenol-based therapies. For example, quercetin (3,3′,4′,5,7-pentahydroxyflavone) is a highly ubiquitous and well-classified dietary polyphenol found in various fruits, vegetables, and other plant products including onions, broccoli, kale, oranges, blueberries, apples, and tea. Quercetin has demonstrated antiproliferative and proapoptotic activity in various cancer cell types. Quercetin is readily metabolized by tyrosinase into various compounds that promote anticancer activity; additionally, given that tyrosinase expression increases during tumorigenesis, and its activity is associated with pigmentation changes in both early- and late-stage melanocytic lesions, it suggests that quercetin can be used to target melanoma. In this review, we explore the potential of quercetin as an anti-melanoma agent utilizing and extrapolating on evidence from previous in vitro studies in various human malignant cell lines and propose a “four-focus area strategy” to develop quercetin as a targeted anti-melanoma compound for use as either a preventative or therapeutic agent. The four areas of focus include utilizing quercetin to (i) modulate cellular bioreduction potential and associated signaling cascades, (ii) affect transcription of relevant genes, (iii) regulate epigenetic processes, and (iv) develop effective combination therapies and delivery modalities/protocols. In general, quercetin could be used to exploit tyrosinase activity to prevent, and/or treat, melanoma with minimal additional side effects.

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Section: Regulation Epigenetic Changessupporting

confidence: 64%

Section: Regulation Epigenetic Changesmentioning

confidence: 98%

Quercetin as an Emerging Anti-Melanoma Agent: A Four-Focus Area Therapeutic Development Strategy

et al. 2016

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“…At present, esophageal cancer ranks the 8th of the incidence of malignant tumors all over the world and patients with esophageal cancer in China takes up more than 50% of the world, with the mobility and cancer related mortality ranking the 4th, highly occurring in Lin County and Anyang City, Hennan Province (Yuan et al, 2014;Malik et al, 2014;Yang et al, 2014;Somi et al, 2014;Zheng et al, 2014). About 50% of patients were found with the advanced period of esophageal cancer when diagnosed, with unfavorable prognosis, about 6~8 months of natural course, 5%~7% five-year survival rate (; Liu et al, 2014;Mai et al, 2014;Zhao et al, 2014;Jiang et al, 2014;Wang et al, 2014;Stefani et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Clinical Observation and Therapeutic Evaluation of Rh-endostatin Combined with DP Regimen in Treating Patients with Advanced Esophageal Cancer

Deng

Song²,

Li³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Objective: To observe the curative effects of rh-endostatin combined with DP regimen in treating patients with advanced esophageal cancer and analyze the correlation of CT perfusion (CTP) parameters and the expression of vascular endothelial growth factor (VEGF). Methods: Twenty patients with esophageal cancer confirmed pathologically were randomly divided into combined treatment (rh-endostatin+DP regimen) group and single chemotherapy group, 10 patients in each group, respectively. All patients were given conventional CT examination and CTP imaging for primary tumor. The level of VEGF, the size of tumor and CTP parameters (BF, BV, PS and MTT) before treatment and after 2 cycles of treatment were determined for the comparison and the correlation between CTP parameters and VEGF expression was analyzed. Results: the therapeutic effect of rh-endostatin+DP regimen group was superior to single chemotherapy group. VEGF level after treatment in rhendostatin +DP regimen group was obviously lower than single chemotherapy group (P<0.01). The expression of VEGF had positive correlation with BF and BV but negative correlation with MTT. Compared with treatment before for rh-endostatin +DP regimen group, BF, BV and PS decreased while MTT increased after treatment (P<0.05). However, there were no significant differences between treatment before and after treatment in single chemotherapy (P>0.05). Conclusions: Rh-endostatin can down-regulate the expression of VEGF in esophageal cancer, change the state of hypertransfusion and high permeability of tumor vessels and had the better curative effect and slighter adverse reactions when combined with chemotherapy.

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“…Additionally, quercetin reduced tumor incidence and induced cell cycle arrest and apoptosis in hamster buccal pouch tumors, and these anticancer properties were correlated with the inhibition of HDAC-1 and DNMT1 (Priyadarsini et al 2011). Combination therapy with quercetin and sodium butyrate suppressed human esophageal 9706 cancer cell (Eca9706) growth in a dose-dependent manner, via downregulation of DNMT1 and HDAC1 which resulted in the increased expression of p16 and E-cadherin (Zheng et al 2014). In prostate cancer cells, quercetin increased antiproliferative activity of EGCG by increasing the bioavailability and decreasing EGCG methylation (Wang et al 2012b).…”

Section: Flavonoidsmentioning

confidence: 99%

Epigenetic Impact of Bioactive Dietary Compounds in Cancer Chemoprevention

Šupić

Wagner

Magić

2016

Critical Dietary Factors in Cancer Chemoprevention

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Epigenetic changes refer to modifications caused by heritable but potentially reversible changes in gene expression not coded in the DNA sequence. Evidence has been provided that various environmental factors and dietary bioactive compounds contribute to cancer development through epigenetic mechanisms. The main mechanisms of epigenetic control in mammals are DNA methylation, histone modifications, and RNA silencing through noncoding RNAs. The inhibition of DNA methyltransferases (DNMTs) involved in DNA methylation of CpG-rich regions of gene promoters and various enzymes involved in the chromatin condensation such as histone deacetylases (HDACs) have been recognized as potent strategies for cancer therapy and chemoprevention. Treatments using natural compounds such as green tea polyphenols, soy isoflavones, curcumin, resveratrol, isothiocyanates, and butyrate (an intestinal product from dietary fiber) modulate DNMT or HDAC gene expression and/or protein levels and activities, indicating that natural compounds could have strong potential to reverse epigenetic changes, without the adverse toxic effects associated with synthetic epigenetic inhibitors used in chemotherapy. Further characterization of the chemopreventive properties of various dietary bioactive compounds is warranted to potentially establish the clinical utility of dietary factors as anticancer compounds either alone or in combination with other dietary factors or clinically relevant therapeutics. Moreover, these characterizations are useful for personalized dietary recommendations and chemopreventive strategies for reducing cancer incidence.

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Aberrant Epigenetic Alteration in Eca9706 Cells Modulated by Nanoliposomal Quercetin Combined with Butyrate Mediated via Epigenetic-NF-κB Signaling

Cited by 37 publications

References 22 publications

Quercetin as an Emerging Anti-Melanoma Agent: A Four-Focus Area Therapeutic Development Strategy

Quercetin as an Emerging Anti-Melanoma Agent: A Four-Focus Area Therapeutic Development Strategy

Clinical Observation and Therapeutic Evaluation of Rh-endostatin Combined with DP Regimen in Treating Patients with Advanced Esophageal Cancer

Epigenetic Impact of Bioactive Dietary Compounds in Cancer Chemoprevention

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