Epigenetic modification of retinoic acid-treated human embryonic stem cells

Cheong, Hyun Sub; Lee, Han Chul; Park, Byung Lae; Kim, Hye Min; Jang, Mi Jin; Han, Yong Mahn; Kim, Seun Young; Kim, Yong‐Sung; Shin, Hyoung Doo

doi:10.5483/bmbrep.2010.43.12.830

Cited by 25 publications

(17 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[1][2][3] Differentiation of ES and EC cells can be induced by retinoic acid (RA). 4,5) Upon RA treatment, NCCIT cells lose their pluripotency, undergo morphological changes, flattening and in some cases acquiring the branched and elongated cytoplasmic processes typical of neurons, and exhibit structural modifications of glycosaminoglycan chains produced via the chondroitin sulfate/dermatan sulfate and heparin/heparin sulfate pathways. 5) Moreover, RA markedly inhibits clonal growth and tumorigenesis in cancer-derived stem cells.…”

Section: Differential Expression Of Ets Family Transcription Factors mentioning

confidence: 99%

Differential Expression of ETS Family Transcription Factors in NCCIT Human Embryonic Carcinoma Cells upon Retinoic Acid-Induced Differentiation

Park

et al. 2014

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

E26 transformation-specific (ETS) transcription factors play important roles in normal and tumorigenic processes during development, differentiation, homeostasis, proliferation, and apoptosis. To identify critical ETS factor(s) in germ cell-derived cancer cells, we examined the expression patterns of the 27 ETS transcription factors in naive and differentiated NCCIT human embryonic carcinoma cells, which exhibit both pluripotent and tumorigenic characteristics. Overall, expression of ETS factors was relatively low in NCCIT cells. Among the 27 ETS factors, polyomavirus enhancer activator 3 (PEA3) and epithelium-specific ETS transcription factor-1 (ESE-1) exhibited the most significant changes in their expression levels. Western blot analysis confirmed these patterns, revealing reduced levels of PEA3 protein and elevated levels of ESE-1 protein in differentiated cells. PEA3 increased the proportion of cells in S-phase and promoted cell growth, whereas ESE-1 reduced proliferation potential. These data suggest that PEA3 and ESE-1 may play important roles in pluripotent and tumorigenic embryonic carcinoma cells. These findings contribute to our understanding of the functions of oncogenic ETS factors in germ cell-derived stem cells during processes related to tumorigenesis and pluripotency.

show abstract

Section: Differential Expression Of Ets Family Transcription Factors mentioning

confidence: 99%

Differential Expression of ETS Family Transcription Factors in NCCIT Human Embryonic Carcinoma Cells upon Retinoic Acid-Induced Differentiation

Park

et al. 2014

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

show abstract

“…Similarly, in MCF-7 breast cancer cells, inhibition of DNMT1 expression by retinoic acid (0.35 M ) led to promoter demethylation and re-expression of RAR ␤ 2 [78] . It has been shown that retinoic acid can further epigenetically modulate targets other than its nuclear receptor [79] . A comprehensive DNA methylation profiling approach of human embryonic stem cells treated with retinoic acid (50 M ) revealed 166 differentially methylated CpG sites and 2,013 differentially expressed genes [79] .…”

Section: Retinoidsmentioning

confidence: 99%

“…It has been shown that retinoic acid can further epigenetically modulate targets other than its nuclear receptor [79] . A comprehensive DNA methylation profiling approach of human embryonic stem cells treated with retinoic acid (50 M ) revealed 166 differentially methylated CpG sites and 2,013 differentially expressed genes [79] . In another study also employing an epigenomic approach in human embryonic stem cells, it was verified that vitamin C (50 g/ml) treatment promoted genome-wide demethylation, but specifically affected a subset of 1,847 genes, including important stem cell genes [80] .…”

Section: Retinoidsmentioning

confidence: 99%

Targeting the Epigenome with Bioactive Food Components for Cancer Prevention

2011

View full text Add to dashboard Cite

Epigenetic processes participate in cancer development and likely influence cancer prevention. Global DNA hypomethylation, gene promoter hypermethylation and aberrant histone posttranslational modifications are hallmarks of neoplastic cells which have been associated with genomic instability and altered gene expression. Because epigenetic deregulation occurs early in carcinogenesis and is potentially reversible, intervention strategies targeting the epigenome have been proposed for cancer prevention. Bioactive food components (BFCs) with anticancer potential, including folate, polyphenols, selenium, retinoids, fatty acids, isothiocyanates and allyl compounds, influence DNA methylation and histone modification processes. Such activities have been shown to affect the expression of genes involved in cell proliferation, death and differentiation that are frequently altered in cancer. Although the epigenome represents a promising target for cancer prevention with BFCs, few studies have addressed the influence of dietary components on these mechanisms in vivo, particularly on the phenotype of humans, and thus the exact mechanisms whereby diet mediates an effect on cancer prevention remains unclear. Primary factors that should be elucidated include the effective doses and dose timing of BFCs to attain epigenetic effects. Because diet-epigenome interactions are likely to occur in utero, the impact of early-life nutrition on cancer risk programming should be further investigated.

show abstract

“…Regarding WFIKKN1, it has been reported to be overexpressed in response to various compounds (Table 3) such as polycyclic aromatic hydrocarbons in zebrafish [54], retinoic acid in human embryonic stem cells [55], the caspase inhibitor RBC1023 [56] in mice and the gastric inhibitory polypeptide in rats [57]. The WFIKKN1 gene is also downregulated in mouse embryonic stem cells overexpressing the N-terminal domain of the Dnmt3a1 DNA methyltransferase probably via epigenetic silencing [58].…”

Section: Wfikkn Expression In Other Tissues or Cell Linesmentioning

confidence: 99%