Hypermethylation of the PTEN gene in ovarian cancer cell lines

Schöndorf, Thomas; Ebert, Matthias P.; Hoffmann, Juliane; Becker, Martina; Moser, Natasha; Pur, Şaziye; Göhring, Uwe-Jochen; Weisshaar, Maria-Paz

doi:10.1016/j.canlet.2003.10.028

Cited by 34 publications

(18 citation statements)

References 20 publications

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“…The mechanism of down-regulation of PTEN was thought to be promoter hypermethylation. However, the demethylation agent 5-aza-2 ¶-deoxycytidine failed to restore PTEN protein expression, suggesting that PTEN is highly regulated at the translational level and that methylation of the PTEN gene plays a subordinate role in ovarian cancer (32). In the present study, we showed that PTEN is negatively regulated by miR-214 at the protein level and that down-regulation of PTEN largely correlates with elevated levels of miR-214 in ovarian cancer (Fig.…”

Section: Discussionmentioning

confidence: 49%

MicroRNA Expression Profiling in Human Ovarian Cancer: miR-214 Induces Cell Survival and Cisplatin Resistance by Targeting PTEN

et al. 2008

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MicroRNAs (miRNA) represent a novel class of genes that function as negative regulators of gene expression. Recently, miRNAs have been implicated in several cancers. However, aberrant miRNA expression and its clinicopathologic significance in human ovarian cancer have not been well documented. Here, we show that several miRNAs are altered in human ovarian cancer, with the most significantly deregulated miRNAs being miR-214, miR-199a*, miR-200a, miR-100, miR125b, and let-7 cluster. Further, we show the frequent deregulation of miR-

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Section: Discussionmentioning

confidence: 49%

MicroRNA Expression Profiling in Human Ovarian Cancer: miR-214 Induces Cell Survival and Cisplatin Resistance by Targeting PTEN

et al. 2008

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“…The gene methylation frequencies observed in TMS1, APC and MINT31 in our study were comparable with the previous studies, whilst the methylation frequencies in this study are higher for RAR 2 and HIC1 but lower for P15 and P16 (Makarla et al 2005;Rathi et al 2002;Strathdee et al 2001;Terasawa et al 2004). Methylation in PTEN was reported in cell lines but not ovarian tumor tissues (Schondorf et al 2004). Methylation of RIZ1 has not been reported previously in any type of ovarian tumors.…”

Section: Discussionmentioning

confidence: 99%

Methylation profile in benign, borderline and malignant ovarian tumors

Tam

Liu

et al. 2006

J Cancer Res Clin Oncol

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“…DNA methylation refers to the addition of a methyl group to the cytosine-5 position of a CpG dinucleotide that is controlled by DNA methyltransferases. There are well described cases of gene regulation in ovarian cancer relying on hyper- or hypomethylation, including down-regulation of both BRCA1 and the PTEN tumor suppressors by promoter hypermethylation (27, 28). Of note, the cell surface marker CD133 that is part of a panel used to define ovarian cancer-initiating cells has been shown to be regulated by both histone modification and promoter methylation (29).…”

Section: Epigenomics and Seoc Unlocking New Opportunities For Therapymentioning

confidence: 99%

Histones and Their Modifications in Ovarian Cancer â€“ Drivers of Disease and Therapeutic Targets

2014

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Epithelial ovarian cancer has the highest mortality of the gynecological malignancies. High grade serous epithelial ovarian cancer (SEOC) is the most common subtype, with the majority of women presenting with advanced disease where 5-year survival is around 25%. Platinum-based chemotherapy in combination with paclitaxel remains the most effective treatment despite platinum therapies being introduced almost 40 years ago. Advances in molecular medicine are underpinning new strategies for the treatment of cancer. Major advances have been made by international initiatives to sequence cancer genomes. For SEOC, with the exception of TP53 that is mutated in virtually 100% of these tumors, there is no other gene mutated at high frequency. There is extensive copy number variation, as well as changes in methylation patterns that will influence gene expression. To date, the role of histones and their post-translational modifications in ovarian cancer is a relatively understudied field. Post-translational histone modifications play major roles in gene expression as they direct the configuration of chromatin and so access by transcription factors. Histone modifications include methylation, acetylation, and monoubiquitination, with involvement of enzymes including histone methyltransferases, histone acetyltransferases/deacetylases, and ubiquitin ligases/deubiquitinases, respectively. Complexes such as the Polycomb repressive complex also play roles in the control of histone modifications and more recently roles for long non-coding RNA and microRNAs are emerging. Epigenomic-based therapies targeting histone modifications are being developed and offer new approaches for the treatment of ovarian cancer. Here, we discuss histone modifications and their aberrant regulation in malignancy and specifically in ovarian cancer. We review current and upcoming histone-based therapies that have the potential to inform and improve treatment strategies for women with ovarian cancer.

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Hypermethylation of the PTEN gene in ovarian cancer cell lines

Cited by 34 publications

References 20 publications

MicroRNA Expression Profiling in Human Ovarian Cancer: miR-214 Induces Cell Survival and Cisplatin Resistance by Targeting PTEN

MicroRNA Expression Profiling in Human Ovarian Cancer: miR-214 Induces Cell Survival and Cisplatin Resistance by Targeting PTEN

Methylation profile in benign, borderline and malignant ovarian tumors

Histones and Their Modifications in Ovarian Cancer â€“ Drivers of Disease and Therapeutic Targets

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