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  • 1
    Online Resource
    Online Resource
    Characterization of DNA methylation of the promoters CTCF and BORIS ( CTCFL ) in breast and ovarian cancer.
    American Society of Clinical Oncology (ASCO) ; 2013
    In:  Journal of Clinical Oncology Vol. 31, No. 15_suppl ( 2013-05-20), p. e22151-e22151
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 31, No. 15_suppl ( 2013-05-20), p. e22151-e22151
    Abstract: e22151 Background: Genetic and epigenetic alterations may promote the initiation or development of cancer. Global DNA hypomethylation and local hypermethylation have been observed, particularly in cell cycle control-associated genes, such as tumor suppressor genes like CTCF. The dissociation of CTCF is associated with hypermethylation of several promoters; its paralogue gene (BORIS) is normally expressed in testicular tissue during spermatogenesis. BORIS over-expression has been identified in multiple neoplasms such as melanoma, gynecological cancer, glioblastoma and – recently – breast cancer. The aim of this study was to characterize the methylation status of the promoter regions of CTCF and BORIS in samples from breast and ovarian cancer compared to non-neoplastic tissue, and correlate it to its expression. Methods: Tissue samples from breast and ovarian cancer, as well as healthy controls were analyzed by MS-PCR for CTCF and BORIS. BorismRNA expression was also analyzed by RT-PCR. Results: A total of 8 ovarian and 16 breast tumors, as well as 10 tumor-adjacent breast tissue samples were prospectively obtained. In non-neoplastic tissue, BORIS was found to be hypermethylated, while in ovarian tumors a loss of methylation was identified in 75% of the samples. The same phenomenon was observed in 68% of breast cancer samples when compared to non-neoplastic tissue. A correlation between loss of DNA methylation of the promoter and gene over-expression was found by RT-PCR, thus suggesting that methylation is an epigenetic phenomenon associated to the over-expression of the oncogene BORIS. The methylation analysis of CTCF did not show any differences between neoplastic and non-neoplastic tissue, suggesting that epigenetic changes mainly affect BORIS. Conclusions: Loss of methylation of the promoter region of BORIS is associated with the over-expression of the gene. No differences were found in the methylation status between healthy and neoplastic tissue for CTCF.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2013.31.15_suppl.e22151
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2013
    detail.hit.zdb_id: 2005181-5
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  • 2
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    Disruption of CTCF at the miR-125b1 locus in gynecological cancers
    Springer Science and Business Media LLC ; 2012
    In:  BMC Cancer Vol. 12, No. 1 ( 2012-12)
    Details
    In: BMC Cancer, Springer Science and Business Media LLC, Vol. 12, No. 1 ( 2012-12)
    Abstract: In cancer cells, transcriptional gene silencing has been associated with genetic and epigenetic defects. The disruption of DNA methylation patterns and covalent histone marks has been associated with cancer development. Until recently, microRNA (miRNA) gene silencing was not well understood. In particular, miR-125b1 has been suggested to be an miRNA with tumor suppressor activity, and it has been shown to be deregulated in various human cancers. In the present study, we evaluated the DNA methylation at the CpG island proximal to the transcription start site of miR-125b1 in cancer cell lines as well as in normal tissues and gynecological tumor samples. In addition, we analyzed the association of CTCF and covalent histone modifications at the miR-125b1 locus. Methods To assess the DNA methylation status of the miR-125b1, genomic DNA was transformed with sodium bisulfite, and then PCR-amplified with modified primers and sequenced. The miR-125b1 gene expression was analyzed by qRT-PCR using U6 as a control for constitutive gene expression. CTCF repressive histone marks abundance was evaluated by chromatin immunoprecipitation assays. Results The disruption of CTCF in breast cancer cells correlated with the incorporation of repressive histone marks such H3K9me3 and H3K27me3 as well as with aberrant DNA methylation patterns. To determine the effect of DNA methylation at the CpG island of miR-125b1 on the expression of this gene, we performed a qRT-PCR assay. We observed a significant reduction on the expression of miR-125b1 in cancer cells in comparison with controls, suggesting that DNA methylation at the CpG island might reduce miR-125b1 expression. These effects were observed in other gynecological cancers, including ovarian and cervical tumors. Conclusions A reduction of miR-125b1 expression in cancers, correlated with methylation, repressive histone marks and loss of CTCF binding at the promoter region.
    Type of Medium: Online Resource
    ISSN: 1471-2407
    URL: Article
    DOI: 10.1186/1471-2407-12-40
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2012
    detail.hit.zdb_id: 2041352-X
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  • 3
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    Disruption of CTCF at the miR-125b1 locus in gynecological cancers and breast cancer cell lines
    Springer Science and Business Media LLC ; 2013
    In:  Epigenetics & Chromatin Vol. 6, No. S1 ( 2013-3)
    Details
    In: Epigenetics & Chromatin, Springer Science and Business Media LLC, Vol. 6, No. S1 ( 2013-3)
    Type of Medium: Online Resource
    ISSN: 1756-8935
    URL: Article
    DOI: 10.1186/1756-8935-6-S1-P79
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2013
    detail.hit.zdb_id: 2462129-8
    SSG: 15,3
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  • 4
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    Abstract 5041: Characterization of the miR-125b1 promoter in breast cancer cell lines
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 5041-5041
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 5041-5041
    Abstract: In cancer cells, transcriptional gene silencing has been associated with genetic and epigenetic defects. The disruption of DNA methylation patterns and covalent histone marks has been associated with cancer development. Until recently, microRNA (miRNA) gene silencing was not well understood. In particular, miR-125b1 has been suggested to be a miRNA with tumor suppressor activity, and it has been shown to be deregulated in various human cancers. In this study, we characterized the promoter of the miR-125b1 and the modifications associated with gene silencing. We studied in silico the miR-125b1 locus to delimit the promoter region and then, we characterized the promoter activity by the luciferase assay, cloning a fragment in the 5′ extreme close to the transcriptional start site of the miR-125b1 gene. We found that this sequence has promoter activity and it is unidirectional. Subsequently, we analyzed the DNA methylation status in the CpG island promoter and found that it was methylated in breast cancer cell lines compared with a non-transformed breast cell line. To determine the effect of DNA methylation in the CpG island of miR-125b1 on the expression of this gene, we performed a qRT-PCR assay. We observed a significant reduction on the expression of miR-125b1 in cancer cells lines in comparison with a non-transformed cell line, suggesting that DNA methylation at the CpG island might reduce the expression of miR-125b1. Our data suggest that the fragment in the 5′ extreme close to the transcriptional start site of the miR-125b1 gene is a functional and unidirectional promoter. Also, the CpG island in this region is methylated in breast cancer cell lines and this methylation is associated with the silencing of the miR-125b1 gene. This work was supported by the Consejo Nacional de Ciencia y Tecnología (CONACyT: 83959) and the Programa de Apoyo a Proyectos de Investigación e Innovación Tecnológica of the Universidad Nacional Autónoma de México (PAPIIT, IN213311). Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5041. doi:1538-7445.AM2012-5041
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-5041
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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