Aberrant methylation of human L- and M-fructose 1,6-bisphosphatase genes in cancer
A possible epigenetic regulation of the two isoenzymes of fructose 1,6-bisphosphatase (FBPase) was studied in liver, muscle, mamma, breast cancer and in different cancer cell lines. Results obtained after bisulfite sequencing revealed a different CpG methylation of both promoters in liver, muscle an...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2008-12, Vol.377 (2), p.720-724 |
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| creator | Bigl, Marina Jandrig, Burkhard Horn, Lars-Christian Eschrich, Klaus |
| description | A possible epigenetic regulation of the two isoenzymes of fructose 1,6-bisphosphatase (FBPase) was studied in liver, muscle, mamma, breast cancer and in different cancer cell lines. Results obtained after bisulfite sequencing revealed a different CpG methylation of both promoters in liver, muscle and breast tissue which is putatively involved in the cell-type specific gene expression of the two enzymes. In tumor cell lines, demethylation with 5-aza-deoxycytidine activated the expression of both isoenzymes. Additional inhibition of histone deacetylase with trichostatin A further increased FBPase mRNA concentrations. Since cancers typically have an abnormal energy metabolism and exhibit a low gluconeogenic phenotype, it was studied whether promoter methylation contributes to the decreased expression of FBPase in breast cancer. When non-malignant and malignant tissue samples from the same patient were compared a correlation between an increase of FBPase promoter methylation and a decrease of FBPase mRNA levels was observed. |
| doi_str_mv | 10.1016/j.bbrc.2008.10.045 |
| format | Article |
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Results obtained after bisulfite sequencing revealed a different CpG methylation of both promoters in liver, muscle and breast tissue which is putatively involved in the cell-type specific gene expression of the two enzymes. In tumor cell lines, demethylation with 5-aza-deoxycytidine activated the expression of both isoenzymes. Additional inhibition of histone deacetylase with trichostatin A further increased FBPase mRNA concentrations. Since cancers typically have an abnormal energy metabolism and exhibit a low gluconeogenic phenotype, it was studied whether promoter methylation contributes to the decreased expression of FBPase in breast cancer. 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Results obtained after bisulfite sequencing revealed a different CpG methylation of both promoters in liver, muscle and breast tissue which is putatively involved in the cell-type specific gene expression of the two enzymes. In tumor cell lines, demethylation with 5-aza-deoxycytidine activated the expression of both isoenzymes. Additional inhibition of histone deacetylase with trichostatin A further increased FBPase mRNA concentrations. Since cancers typically have an abnormal energy metabolism and exhibit a low gluconeogenic phenotype, it was studied whether promoter methylation contributes to the decreased expression of FBPase in breast cancer. When non-malignant and malignant tissue samples from the same patient were compared a correlation between an increase of FBPase promoter methylation and a decrease of FBPase mRNA levels was observed.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Azacitidine - pharmacology</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - enzymology</subject><subject>Breast Neoplasms - genetics</subject><subject>Cell line</subject><subject>Cell Line, Tumor</subject><subject>DNA methylation</subject><subject>DNA Methylation - drug effects</subject><subject>Female</subject><subject>Fructose 1,6-bisphosphatase</subject><subject>Fructose-Bisphosphatase - genetics</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Silencing</subject><subject>Gluconeogenesis</subject><subject>Humans</subject><subject>Hydroxamic Acids - pharmacology</subject><subject>Middle Aged</subject><subject>Neoplasms - enzymology</subject><subject>Neoplasms - genetics</subject><subject>Promoter</subject><subject>Promoter Regions, Genetic</subject><subject>Tissue-specific expression</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LAzEQhoMotlb_gAfJyZNbk81udgNepPgFFUF68BayyaxN2Y-aZIX-e7O04E0Pw8DLMy_Dg9AlJXNKKL_dzKvK6XlKSBmDOcnyIzSlRJAkpSQ7RlNCCE9SQT8m6Mz7DSGUZlycogktBSspE1P0fl-Bc6oLuIWw3jUq2L7DfY3XQ6s6vEyw6gx-TWo36NB7wPSGJ5X123UfRwUVo0_owGPbYa06De4cndSq8XBx2DO0enxYLZ6T5dvTy-J-mWhW5iFhtRI5L9P4iuKaKqEzVnGmCigYVJrljBhWG2EKroAYlRkDnKVQc2B5nbIZut7Xbl3_NYAPsrVeQ9OoDvrBSy6Kko3t_4FU8DTLKY1guge16713UMuts61yO0mJHI3LjRyNy9H4mEXj8ejq0D5ULZjfk4PiCNztAYguvi046bWFKMpYBzpI09u_-n8A-maRjg</recordid><startdate>20081212</startdate><enddate>20081212</enddate><creator>Bigl, Marina</creator><creator>Jandrig, Burkhard</creator><creator>Horn, Lars-Christian</creator><creator>Eschrich, Klaus</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20081212</creationdate><title>Aberrant methylation of human L- and M-fructose 1,6-bisphosphatase genes in cancer</title><author>Bigl, Marina ; Jandrig, Burkhard ; Horn, Lars-Christian ; Eschrich, Klaus</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c385t-3fa95682893a6c1a9c43b63a7e73ebc3530d3fd9d76ae0da4dde632ef6e35f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Azacitidine - pharmacology</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - enzymology</topic><topic>Breast Neoplasms - genetics</topic><topic>Cell line</topic><topic>Cell Line, Tumor</topic><topic>DNA methylation</topic><topic>DNA Methylation - drug effects</topic><topic>Female</topic><topic>Fructose 1,6-bisphosphatase</topic><topic>Fructose-Bisphosphatase - genetics</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Enzymologic</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Silencing</topic><topic>Gluconeogenesis</topic><topic>Humans</topic><topic>Hydroxamic Acids - pharmacology</topic><topic>Middle Aged</topic><topic>Neoplasms - enzymology</topic><topic>Neoplasms - genetics</topic><topic>Promoter</topic><topic>Promoter Regions, Genetic</topic><topic>Tissue-specific expression</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bigl, Marina</creatorcontrib><creatorcontrib>Jandrig, Burkhard</creatorcontrib><creatorcontrib>Horn, Lars-Christian</creatorcontrib><creatorcontrib>Eschrich, Klaus</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bigl, Marina</au><au>Jandrig, Burkhard</au><au>Horn, Lars-Christian</au><au>Eschrich, Klaus</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aberrant methylation of human L- and M-fructose 1,6-bisphosphatase genes in cancer</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2008-12-12</date><risdate>2008</risdate><volume>377</volume><issue>2</issue><spage>720</spage><epage>724</epage><pages>720-724</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>A possible epigenetic regulation of the two isoenzymes of fructose 1,6-bisphosphatase (FBPase) was studied in liver, muscle, mamma, breast cancer and in different cancer cell lines. Results obtained after bisulfite sequencing revealed a different CpG methylation of both promoters in liver, muscle and breast tissue which is putatively involved in the cell-type specific gene expression of the two enzymes. In tumor cell lines, demethylation with 5-aza-deoxycytidine activated the expression of both isoenzymes. Additional inhibition of histone deacetylase with trichostatin A further increased FBPase mRNA concentrations. Since cancers typically have an abnormal energy metabolism and exhibit a low gluconeogenic phenotype, it was studied whether promoter methylation contributes to the decreased expression of FBPase in breast cancer. When non-malignant and malignant tissue samples from the same patient were compared a correlation between an increase of FBPase promoter methylation and a decrease of FBPase mRNA levels was observed.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>18938139</pmid><doi>10.1016/j.bbrc.2008.10.045</doi><tpages>5</tpages></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Azacitidine - pharmacology Breast cancer Breast Neoplasms - enzymology Breast Neoplasms - genetics Cell line Cell Line, Tumor DNA methylation DNA Methylation - drug effects Female Fructose 1,6-bisphosphatase Fructose-Bisphosphatase - genetics Gene expression Gene Expression Regulation, Enzymologic Gene Expression Regulation, Neoplastic Gene Silencing Gluconeogenesis Humans Hydroxamic Acids - pharmacology Middle Aged Neoplasms - enzymology Neoplasms - genetics Promoter Promoter Regions, Genetic Tissue-specific expression |
| title | Aberrant methylation of human L- and M-fructose 1,6-bisphosphatase genes in cancer |
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