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miRNA-218 contributes to the regulation of D-glucuronyl C5-epimerase expression in normal and tumor breast tissues
Russian Academy of Medical Science, Russia .
Russian Academy of Medical Science, Russia.
Ukrainian National Academy of Science, Ukraine .
Karolinska Institute, Sweden .
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2012 (English)In: Epigenetics, ISSN 1559-2294, E-ISSN 1559-2308, Vol. 7, no 10, 1109-1114 p.Article in journal (Refereed) Published
Abstract [en]

microRNAs (miRNAs) are key posttranscriptional regulators of gene expression. In the present study, regulation of tumor-suppressor gene D-glucuronyl C5-epimerase (GLCE) by miRNA-218 was investigated. Significant downregulation of miRNA-218 expression was shown in primary breast tumors. Exogenous miRNA-218/anti-miRNA-218 did not affect GLCE mRNA but regulated GLCE protein level in MCF7 breast carcinoma cells in vitro. Comparative analysis showed a positive correlation between miRNA-218 and GLCE mRNA, and negative correlation between miRNA-218 and GLCE protein levels in breast tissues and primary tumors in vivo, supporting a direct involvement of miRNA-218 in posttranscriptional regulation of GLCE in human breast tissue. A common scheme for the regulation of GLCE expression in normal and tumor breast tissues is suggested.

Place, publisher, year, edition, pages
Landes Bioscience , 2012. Vol. 7, no 10, 1109-1114 p.
Keyword [en]
miRNA, D-glucuronyl C5-epimerase, GLCE, tumor-suppressor gene, expression, heparan sulphate proteoglycan, biosynthesis, breast cancer
National Category
Engineering and Technology
URN: urn:nbn:se:liu:diva-85632DOI: 10.4161/epi.22103ISI: 000309960600003OAI: diva2:572053

Funding Agencies|Russian Foundation for Basic Research|11-04-90400-Ukr_f_a|Ukranian State Foundation of Fundamental Research|F40/146-2011F46/457-2011|Swedish Institute|2011/00888|UICC International Cancer Technology Transfer Fellowship|ICRETT-09-069|FEBS Short-term Fellowship||Karolinska Institute||Swedish Cancer Society||Swedish Research Council||

Available from: 2012-11-26 Created: 2012-11-26 Last updated: 2014-10-28

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