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Genistein inhibits DNA methylation and increases expression of tumor suppressor genes in human breast cancer cells
Genes chromosomes & cancer, 2014-05, Vol.53 (5), p.422-431
Xie, Qi
Bai, Qian
Zou, Ling-Yun
Zhang, Qian-Yong
Zhou, Yong
Chang, Hui
Yi, Long
Zhu, Jun-Dong
Mi, Man-Tian
2014
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Xie, Qi
Bai, Qian
Zou, Ling-Yun
Zhang, Qian-Yong
Zhou, Yong
Chang, Hui
Yi, Long
Zhu, Jun-Dong
Mi, Man-Tian
Titel
Genistein inhibits DNA methylation and increases expression of tumor suppressor genes in human breast cancer cells
Ist Teil von
Genes chromosomes & cancer, 2014-05, Vol.53 (5), p.422-431
Ort / Verlag
United States: Blackwell Publishing Ltd
Erscheinungsjahr
2014
Quelle
MEDLINE
Beschreibungen/Notizen
It has been previously demonstrated that genistein exhibits anticancer activity against breast cancer. However, the precise mechanisms underlying the anticancer effect of genistein, in particular the epigenetic basis, remain unclear. In this study, we investigated whether genistein could modulate the DNA methylation status and expression of cancer‐related genes in breast cancer cells. We treated MCF‐7 and MDA‐MB‐231 human breast cancer cells with genistein in vitro. We found that genistein decreased the levels of global DNA methylation, DNA methyltransferase (DNMT) activity and expression of DNMT1. Yet, the expression of DNMT3A and DNMT3B showed no significant change. Using molecular modeling, we observed that genistein might directly interact with the catalytic domain of DNMT1, thus competitively inhibiting the binding of hemimethylated DNA to the catalytic domain of DNMT1. Furthermore, genistein decreased DNA methylation in the promoter region of multiple tumor suppressor genes (TSGs) such as ataxia telangiectasia mutated (ATM), adenomatous polyposis coli (APC), phosphatase and tensin homolog (PTEN), mammary serpin peptidase inhibitor (SERPINB5), and increased the mRNA expression of these genes. However, we detected no significant changes in the DNA methylation status or mRNA expression of stratifin (SFN). These results suggest that the anticancer effect of genistein on breast cancer may be partly due to its ability to demethylate and reactivate methylation‐silenced TSGs through direct interaction with the DNMT1 catalytic domain and inhibition of DNMT1 expression. © 2014 Wiley Periodicals, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 1045-2257
eISSN: 1098-2264
DOI: 10.1002/gcc.22154
Titel-ID: cdi_proquest_miscellaneous_1512327242
Format
–
Schlagworte
Antineoplastic Agents - pharmacology
,
Breast Neoplasms - genetics
,
Breast Neoplasms - metabolism
,
Breast Neoplasms - pathology
,
Cell Line, Tumor - drug effects
,
Cell Survival - drug effects
,
DNA (Cytosine-5-)-Methyltransferase 1
,
DNA (Cytosine-5-)-Methyltransferases - genetics
,
DNA (Cytosine-5-)-Methyltransferases - metabolism
,
DNA Methylation - drug effects
,
Epigenesis, Genetic
,
Female
,
Genes, Tumor Suppressor
,
Genistein - pharmacology
,
Genome, Human
,
Humans
,
Models, Molecular
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