Epigenome, Cancer Prevention and Flavonoids and Curcumin

Stepanić, Višnja; Kujundžić, Renata Novak; Trošelj, Koraljka Gall

doi:10.5772/58247

Cited by 10 publications

(10 citation statements)

References 146 publications

(204 reference statements)

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“…We observed a statistically significant decrease of ERBB1 (EGFR) gene involved in cells' differentiation and proliferation after morin hydrate and all compounds treatment. Additionally, our results have shown a statistically significant decrease of TMEF1 and TMEM132A genes considered as up-regulated during EMT after all used compounds [8,10,23]. Analysis of expression of genes involved in EMT in SKOV-3 cells have shown statistically significant decrease of genes involved in cell migration and motility: AHNAK, FN1, and STAT3 after morin hydrate and all used compounds, and MST1R after decitabine and decitabine with trichostatin A.…”

Section: Measurement Of Transcriptomic Responses To Morin Hydrate In supporting

confidence: 57%

“…Similar results observed Xie Q et al in MCF-7 and MDA-MB-231 human breast cancer cells treated with genistein (100 μM) in vitro. Noteworthy, morin hydrate as a catechol polyphenol, may indirectly inhibit DNMTs and DNA methylation, through changing intracellular concentrations of S-adenosyl methionine (SAM) [23,[37][38][39]. Hypomethylation and hypermethylation are found in the same tumor although in the different sequences, it had been noticed that there is a dependence between demethylation and de novo methylation mechanisms during tumorigenesis [38].…”

Section: Discussionmentioning

confidence: 99%

“…Some of the flavonols, e.g., quercetin or fisetin, highly structurally similar to morin, were tested for DNMT inhibition, and all inhibited DNMT1-mediated DNA methylation. Additionally, quercetin causes HAT activation and HDAC inhibition [22,23].…”

Section: Epigenetic Modulation Of Emt: Natural Compounds As An Alternmentioning

confidence: 99%

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Morin exerts anti-metastatic, anti-proliferative and anti-adhesive effect in ovarian cancer cells: an in vitro studies

2020

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The influence of morin hydrate on changes of proliferative, metastatic, and adhesive potential of human ovarian cancer cells concerning the influence of decitabine, and decitabine with trichostatin A, and in comparison to untreated cells, were analyzed. The effect of morin hydrate, decitabine, and trichostatin A were examined in A2780 and SKOV-3 ovarian cancer cell lines using MTS assay, clonogenic assay, adhesion to endothelial HMEC-1 cells, transwell migration assay and cell cycle analysis. The expression level of epithelial to mesenchymal transition (EMT) markers was quantified using PCR Array in relation to the level of global methylation determined with Methylated DNA Quantification Kit. We observed statistically significant inhibition of adhesive and migratory potential of both cell lines and the accumulation of G0/G1 phase A2780 cells after treatment with morin hydrate. Our studies confirmed the influence of morin hydrate on down-regulation of genes considered as up-regulated during EMT, and up-regulation of some genes considered as down-regulated during EMT in A2780 and SKOV-3 cells. Phenotypic changes were associated with molecular changes in cells, eg. decrease of the expression level of genes associated with adhesion, and an increase of genes down-regulated during EMT, after morin hydrate treatment in comparison to untreated control cells in both cell lines, were observed. Keywords Adhesion • Epithelial to mesenchymal transition • Metastasis • Morin hydrate • Ovarian cancer cells Abbreviations ATCC American type culture collection DNMT DNA methyltransferase ECACC European collection of authenticated cell cultures ECM Extracellular matrix EMT Epithelial to mesenchymal transition EOC Epithelial ovarian cancer HAT Histone acetyltransferase HDAC Histone deacetylase MET Mesenchymal to epithelial transition SAM S-sdenosyl-l-methionine TSA Trichostatin A

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Section: Measurement Of Transcriptomic Responses To Morin Hydrate In supporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

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Morin exerts anti-metastatic, anti-proliferative and anti-adhesive effect in ovarian cancer cells: an in vitro studies

2020

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“…Quercetin has been shown to slow down carcinogenesis through inhibition of a pro-proliferative signaling pathway, both in animal models and in human cancer cell lines [135][136][137].…”

Section: Flavonolsmentioning

confidence: 99%

Flavonoids as Epigenetic Modulators for Prostate Cancer Prevention

2020

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Prostate cancer (PCa) is a multifactorial disease with an unclear etiology. Due to its high prevalence, long latency, and slow progression, PCa is an ideal target for chemoprevention strategies. Many research studies have highlighted the positive effects of natural flavonoids on chronic diseases, including PCa. Different classes of dietary flavonoids exhibit anti-oxidative, anti-inflammatory, anti-mutagenic, anti-aging, cardioprotective, anti-viral/bacterial and anti-carcinogenic properties. We overviewed the most recent evidence of the antitumoral effects exerted by dietary flavonoids, with a special focus on their epigenetic action in PCa. Epigenetic alterations have been identified as key initiating events in several kinds of cancer. Many dietary flavonoids have been found to reverse DNA aberrations that promote neoplastic transformation, particularly for PCa. The epigenetic targets of the actions of flavonoids include oncogenes and tumor suppressor genes, indirectly controlled through the regulation of epigenetic enzymes such as DNA methyltransferase (DNMT), histone acetyltransferase (HAT), and histone deacetylase (HDAC). In addition, flavonoids were found capable of restoring miRNA and lncRNA expression that is altered during diseases. The optimization of the use of flavonoids as natural epigenetic modulators for chemoprevention and as a possible treatment of PCa and other kinds of cancers could represent a promising and valid strategy to inhibit carcinogenesis and fight cancer.

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“…The cellular defense against the oxidative stress is mainly achieved by activation of the nuclear factor E2-related factor 2/antioxidant response element (Nrf2/ARE) signaling pathway [7,8,9]. Most chemopreventive compounds including dietary phytochemicals have been reported to remove intracellular ROS by increasing the expression of genes involved in the antioxidant defense system, which, in turn, is activated by Nrf2, a transcription factor liberated from Kelch-like ECH-associated protein 1 (Keap1), translocated to the nucleus, and subsequently bound to the ARE of target genes [10,11,12].…”

Section: Introductionmentioning

confidence: 99%

Luteolin Shifts Oxaliplatin-Induced Cell Cycle Arrest at G0/G1 to Apoptosis in HCT116 Human Colorectal Carcinoma Cells

Jang

Moon

et al. 2019

Nutrients

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Certain antioxidative flavonoids are known to activate nuclear factor E2-related factor 2 (Nrf2), a transcription factor that regulates cellular antioxidants and detoxifying response and is reportedly highly activated in many types of cancers. Few studies on the potential undesired effects of flavonoid intake during chemotherapy have been conducted, yet Nrf2 activators could favor cancer cell survival by attenuating chemotherapeutic efficiency. This study aimed to examine if luteolin, an Nrf2 activator, hinders chemotherapeutic activity of oxaliplatin, a potent anticancer agent for colorectal cancer, in HCT116 cells. Luteolin treatment strongly increased the transcriptional activity of the antioxidant response element in HCT116 cells and induced the protein expression of heme oxygenase-1, which were indicative of its Nrf2-inducing potential. Intriguingly, 25 μM luteolin reduced cell viability through apoptotic induction, which was intensified in p53-expressing cells while 1 μM oxaliplatin caused cell cycle arrest at G0/G1-phase via the p53/p21-dependent mechanism. Moreover, luteolin treatment was found to reduce oxaliplatin-treated p53-null cell viability and colony counts further, thereby demonstrating an additional effect of luteolin in the killing of human colorectal tumor HCT116 cells not expressing functional p53 protein. The findings suggest that luteolin can induce p53-mediated apoptosis regardless of oxaliplatin treatment and may eliminate oxaliplatin-resistant p53-null colorectal cells.

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Epigenome, Cancer Prevention and Flavonoids and Curcumin

Cited by 10 publications

References 146 publications

Morin exerts anti-metastatic, anti-proliferative and anti-adhesive effect in ovarian cancer cells: an in vitro studies

Morin exerts anti-metastatic, anti-proliferative and anti-adhesive effect in ovarian cancer cells: an in vitro studies

Flavonoids as Epigenetic Modulators for Prostate Cancer Prevention

Luteolin Shifts Oxaliplatin-Induced Cell Cycle Arrest at G0/G1 to Apoptosis in HCT116 Human Colorectal Carcinoma Cells

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