The Roles of Retinoic Acid and Retinoic Acid Receptors in Inducing Epigenetic Changes

Urvalek, Alison M.; Laursen, Kristian B.; Gudas, Lorraine J.

doi:10.1007/978-94-017-9050-5_7

Cited by 44 publications

(46 citation statements)

References 104 publications

(142 reference statements)

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“…Hence, SIN3B, HDAC1 and HDAC2 could constitute the interaction nodes that link MYT1 to other proteins involved in craniofacial development, as suggested by in silico analysis of protein network (see figure 4B and see online supplementary table S3). In HDAC1 knockdown cells, an increase of RARB expression has been shown 48. Thus, the SIN3B-HDAC1-MYT1 complex could modulate the RA pathway by the regulation of RARB expression.…”

Section: Discussionmentioning

confidence: 97%

Mutations inMYT1, encoding the myelin transcription factor 1, are a rare cause of OAVS

et al. 2016

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Section: Discussionmentioning

confidence: 97%

Mutations inMYT1, encoding the myelin transcription factor 1, are a rare cause of OAVS

et al. 2016

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“…Histone tails are subjected to many different posttranslational modifications that can alter gene expression (Hon et al, 2009, Urvalek et al, 2014), and aberrant epigenetic modifications are found in both early and late stages of carcinogenesis (Chen et al, 2011). In hepatocytes ethanol can affect these epigenetic changes, potentially by regulating the availability of substrates for epigenetic modifications, including acetyl-CoA (for acetylation) and S-andenosyl-methionine (for methylation) (Shukla et al, 2008, Seitz and Stickel, 2007, Seitz and Becker, 2007).…”

Section: Resultsmentioning

confidence: 99%

“…Histone tails are subjected to a multitude of post-translational modifications that can mark a gene promoter as being in an active or inactive state (Shukla et al, 2008). Acetylation at histone 3 lysine residues 9, 14, and 27, (H3K9/14ac or H3K27ac) and mono-methylation at histone 3 lysine 4 (H3K4me1) are typically associated with increased gene expression (Shukla et al, 2008, Urvalek et al, 2014). Conversely, tri-methylation at lysine 27 or 9 of histone 3 (H3K27me3 and H3K9me3) is associated with epigenetic silencing (Shukla et al, 2008, Urvalek and Gudas, 2014).…”

Section: Introductionmentioning

confidence: 99%

Identification of Ethanol and 4-Nitroquinoline-1-Oxide Induced Epigenetic and Oxidative Stress Markers During Oral Cavity Carcinogenesis

Urvalek

Osei-Sarfo

Tang

et al. 2015

Alcohol Clin Exp Res

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Background Head and neck squamous cell carcinoma (HNSCC) is a cancer that is characterized by its high morbidity and mortality rates. While tobacco use and alcohol consumption are two major contributing factors for HNSCC carcinogenesis, how the combination of tobacco and alcohol increases HNSCC risk is not understood. Methods We combined the 4-nitroquinoline-1-oxide (4-NQO) oral carcinogenesis and Meadows-Cook alcohol mouse models to elucidate the molecular events and to identify novel biomarkers associated with oral cancer development. Results By genome-wide RNA-seq of tongue samples (three mice per group) we identified changes in transcripts that mediate alcohol metabolism and oxidative stress (Aldh2, Aldh1a3, Adh1, Adh7, and Cyp2a5) in mice treated with 4-NQO followed by ethanol (4-NQO/EtOH) as compared to the vehicle control/untreated samples (V.C./Untr.). We measured major, global increases in specific histone acetylation and methylation epigenetic marks (H3K27ac, H3K9/14ac, H3K27me3, and H3K9me3) in the oral cavities of V.C./EtOH, 4-NQO/Untr. and 4-NQO/EtOH treatment groups compared to the V.C./Untr. group. We detected changes in histone epigenetic marks near regulatory regions of genes involved in ethanol metabolism by chromatin immunoprecipitation (ChIP). For instance, the Aldh2 promoter showed increased H3K27me3 marks, and Aldh2 mRNA levels were reduced by 10-fold in 4NQO/EtOH vs. V.C./Untr. tongue samples. 4-NQO/EtOH treatment also caused increases in markers of oxidative stress, including 4-HNE, MCT4/Slc16a3, and TOM20, as measured by immunohistochemistry. Conclusions We delineate a mechanism by which 4-NQO and ethanol can regulate gene expression during the development of HNSCC, and suggest that histone epigenetic marks and oxidative stress markers could be novel biomarkers and targets for the prevention of HNSCC.

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“…It seems that one of these mechanisms is modification of epigenetic alterations (9). The role of ATRA in the modification of epigenetic changes in malignancies has been shown in many studies (17). However, the use of ATRA in cancer treatment alone has some limitations (18).…”

Section: Introductionmentioning

confidence: 99%

All-trans retinoic acid and genistein induce cell apoptosis in OVCAR-3 cells by increasing the P14 tumor suppressor gene

Dastjerdi¹,

Zamani²,

Mardani³

et al. 2016

Res Pharma Sci

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In this study, we evaluated the effects of all-trans retinoic acid (ATRA) alone or in combination with genistein (GEN) in p14 tumor suppressor gene and subsequent apoptosis of human ovarian carcinoma cells (OVCAR-3). The cells were treated with ATRA or GEN at concentrations of 50 and 25 μM respectively, either alone or in combination for 24 and 48 h. The cell viability was evaluated using 3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide (MTT) assay. The percentage of cell apoptosis was determined using flow cytometry and p14 gene expression was measured using real time PCR. The MTT results showed that in both ATRA and GEN treated groups, the cell viabilityviability in group treated for 48 h was significantly lower than group treated for 24 h. The flow cytometry results showed that the percentage of apoptotic cells in groups that treated with ATRA and GEN in combination for 24 h and 48 h was significantly more than all other tested groups. The real time results showed that the mRNA level of p14 in cells treated with both drugs for 48 h was significantly higher than all other groups. In conclusion, we confirm that GEN in combination with ATRA is an effective strategy to up regulate the p14 tumor suppressor gene and induce cell apoptosis in OVCAR-3 cell line.

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The Roles of Retinoic Acid and Retinoic Acid Receptors in Inducing Epigenetic Changes

Cited by 44 publications

References 104 publications

Mutations inMYT1, encoding the myelin transcription factor 1, are a rare cause of OAVS

Mutations inMYT1, encoding the myelin transcription factor 1, are a rare cause of OAVS

Identification of Ethanol and 4-Nitroquinoline-1-Oxide Induced Epigenetic and Oxidative Stress Markers During Oral Cavity Carcinogenesis

All-trans retinoic acid and genistein induce cell apoptosis in OVCAR-3 cells by increasing the P14 tumor suppressor gene

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