Increased galectin-7 gene expression in lymphoma cells is under the control of DNA methylation
Recent studies have reported that elevated levels of galectin-7 in different types of cancer. The mechanisms underlying its abnormal regulation in cancer cells remain, however, unknown. Here, we have examined the relationship between galectin-7 and p53, a gene previously associated with upregulation...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2009-09, Vol.387 (3), p.425-429 |
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| creator | Demers, Mélanie Couillard, Julie Giglia-Mari, Giuseppina Magnaldo, Thierry St-Pierre, Yves |
| description | Recent studies have reported that elevated levels of galectin-7 in different types of cancer. The mechanisms underlying its abnormal regulation in cancer cells remain, however, unknown. Here, we have examined the relationship between galectin-7 and p53, a gene previously associated with upregulation of galectin-7. While RNA and protein analyses revealed a consistent and irreversible upregulation of galectin-7 throughout progression of lymphoma, no correlation with p53 was found. In fact, most of the lymphoma cell lines expressing high levels of galectin-7 did not express any detectable level of p53, although expressed
p21
Waf1/Cip1
gene following doxorubicin treatment, indicating that p53 was functional in these cells. Methylation-specific polymerase chain reaction (MS-PCR) analyses rather suggested that galectin-7 expression was associated with changes in DNA methylation. This conclusion was supported by data using demethylating agent 5-aza-dC. Furthermore, disruption of the DNA methylases
dnmt1 and
dnmt3a induced galectin-7. Collectively, our data suggest that abnormal expression of galectin-7 in lymphoma cells is not dependent on p53, but is rather associated with DNA hypomethylation. |
| doi_str_mv | 10.1016/j.bbrc.2009.07.015 |
| format | Article |
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p21
Waf1/Cip1
gene following doxorubicin treatment, indicating that p53 was functional in these cells. Methylation-specific polymerase chain reaction (MS-PCR) analyses rather suggested that galectin-7 expression was associated with changes in DNA methylation. This conclusion was supported by data using demethylating agent 5-aza-dC. Furthermore, disruption of the DNA methylases
dnmt1 and
dnmt3a induced galectin-7. Collectively, our data suggest that abnormal expression of galectin-7 in lymphoma cells is not dependent on p53, but is rather associated with DNA hypomethylation.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2009.07.015</identifier><identifier>PMID: 19596268</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Cell Line, Tumor ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinase Inhibitor p21 - metabolism ; DNA (Cytosine-5-)-Methyltransferase ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases - genetics ; DNA (Cytosine-5-)-Methyltransferases - metabolism ; DNA Methylation ; Galectin-7 ; Galectins ; Galectins - genetics ; Gene Expression ; Gene Expression Regulation, Leukemic ; Human health and pathology ; Humans ; Infectious diseases ; Life Sciences ; Lymphoma ; Lymphoma - genetics ; p53 ; Promoter Regions, Genetic ; Tumor Suppressor Protein p53 ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Biochemical and biophysical research communications, 2009-09, Vol.387 (3), p.425-429</ispartof><rights>2009 Elsevier Inc.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c423t-2ccf21ad60a7d45dd857ac3cece5711f86c784976578720efbf527acd5f27b6d3</citedby><cites>FETCH-LOGICAL-c423t-2ccf21ad60a7d45dd857ac3cece5711f86c784976578720efbf527acd5f27b6d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2009.07.015$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,315,781,785,886,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19596268$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://riip.hal.science/pasteur-00819941$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Demers, Mélanie</creatorcontrib><creatorcontrib>Couillard, Julie</creatorcontrib><creatorcontrib>Giglia-Mari, Giuseppina</creatorcontrib><creatorcontrib>Magnaldo, Thierry</creatorcontrib><creatorcontrib>St-Pierre, Yves</creatorcontrib><title>Increased galectin-7 gene expression in lymphoma cells is under the control of DNA methylation</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Recent studies have reported that elevated levels of galectin-7 in different types of cancer. The mechanisms underlying its abnormal regulation in cancer cells remain, however, unknown. Here, we have examined the relationship between galectin-7 and p53, a gene previously associated with upregulation of galectin-7. While RNA and protein analyses revealed a consistent and irreversible upregulation of galectin-7 throughout progression of lymphoma, no correlation with p53 was found. In fact, most of the lymphoma cell lines expressing high levels of galectin-7 did not express any detectable level of p53, although expressed
p21
Waf1/Cip1
gene following doxorubicin treatment, indicating that p53 was functional in these cells. Methylation-specific polymerase chain reaction (MS-PCR) analyses rather suggested that galectin-7 expression was associated with changes in DNA methylation. This conclusion was supported by data using demethylating agent 5-aza-dC. Furthermore, disruption of the DNA methylases
dnmt1 and
dnmt3a induced galectin-7. Collectively, our data suggest that abnormal expression of galectin-7 in lymphoma cells is not dependent on p53, but is rather associated with DNA hypomethylation.</description><subject>Cell Line, Tumor</subject><subject>Cyclin-Dependent Kinase Inhibitor p21</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</subject><subject>DNA (Cytosine-5-)-Methyltransferase</subject><subject>DNA (Cytosine-5-)-Methyltransferase 1</subject><subject>DNA (Cytosine-5-)-Methyltransferases - genetics</subject><subject>DNA (Cytosine-5-)-Methyltransferases - metabolism</subject><subject>DNA Methylation</subject><subject>Galectin-7</subject><subject>Galectins</subject><subject>Galectins - genetics</subject><subject>Gene Expression</subject><subject>Gene Expression Regulation, Leukemic</subject><subject>Human health and pathology</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Life Sciences</subject><subject>Lymphoma</subject><subject>Lymphoma - genetics</subject><subject>p53</subject><subject>Promoter Regions, Genetic</subject><subject>Tumor Suppressor Protein p53</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkbGO1DAQhi0E4paDF6BArugSxk5ixxLN6g64k1bQgESF5diTW6-SONjJiX17vNoVdFBN8_2_ZuYj5DWDkgET7w5l10VbcgBVgiyBNU_IhoGCgjOon5INAIiCK_b9irxI6QDAWC3Uc3LFVKMEF-2G_LifbEST0NEHM6Bd_FRI-oATUvw1R0zJh4n6iQ7Hcd6H0VCLw5CoT3SdHEa67JHaMC0xDDT09Pbzlo647I-DWXLyJXnWmyHhq8u8Jt8-fvh6c1fsvny6v9nuClvzaim4tT1nxgkw0tWNc20jja0sWmwkY30rrGxrJUUjW8kB-65veCZc03PZCVddk-LcuzeDnqMfTTzqYLy-2-70bNKCa9QALVOqZo8s82_P_BzDzxXTokefTpeZCcOatJBNC_mV_wU58IpXEjLIz6CNIaWI_Z81GOiTLn3QJ136pEuD1FlXDr25tK_diO5v5OInA-_PAObnPXqMOlmPk0XnY5alXfD_6v8NmQmmVw</recordid><startdate>20090925</startdate><enddate>20090925</enddate><creator>Demers, Mélanie</creator><creator>Couillard, Julie</creator><creator>Giglia-Mari, Giuseppina</creator><creator>Magnaldo, Thierry</creator><creator>St-Pierre, Yves</creator><general>Elsevier Inc</general><general>Elsevier</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>7T5</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>1XC</scope></search><sort><creationdate>20090925</creationdate><title>Increased galectin-7 gene expression in lymphoma cells is under the control of DNA methylation</title><author>Demers, Mélanie ; Couillard, Julie ; Giglia-Mari, Giuseppina ; Magnaldo, Thierry ; St-Pierre, Yves</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c423t-2ccf21ad60a7d45dd857ac3cece5711f86c784976578720efbf527acd5f27b6d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Cell Line, Tumor</topic><topic>Cyclin-Dependent Kinase Inhibitor p21</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</topic><topic>DNA (Cytosine-5-)-Methyltransferase</topic><topic>DNA (Cytosine-5-)-Methyltransferase 1</topic><topic>DNA (Cytosine-5-)-Methyltransferases - genetics</topic><topic>DNA (Cytosine-5-)-Methyltransferases - metabolism</topic><topic>DNA Methylation</topic><topic>Galectin-7</topic><topic>Galectins</topic><topic>Galectins - genetics</topic><topic>Gene Expression</topic><topic>Gene Expression Regulation, Leukemic</topic><topic>Human health and pathology</topic><topic>Humans</topic><topic>Infectious diseases</topic><topic>Life Sciences</topic><topic>Lymphoma</topic><topic>Lymphoma - genetics</topic><topic>p53</topic><topic>Promoter Regions, Genetic</topic><topic>Tumor Suppressor Protein p53</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Demers, Mélanie</creatorcontrib><creatorcontrib>Couillard, Julie</creatorcontrib><creatorcontrib>Giglia-Mari, Giuseppina</creatorcontrib><creatorcontrib>Magnaldo, Thierry</creatorcontrib><creatorcontrib>St-Pierre, Yves</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Demers, Mélanie</au><au>Couillard, Julie</au><au>Giglia-Mari, Giuseppina</au><au>Magnaldo, Thierry</au><au>St-Pierre, Yves</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased galectin-7 gene expression in lymphoma cells is under the control of DNA methylation</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2009-09-25</date><risdate>2009</risdate><volume>387</volume><issue>3</issue><spage>425</spage><epage>429</epage><pages>425-429</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Recent studies have reported that elevated levels of galectin-7 in different types of cancer. The mechanisms underlying its abnormal regulation in cancer cells remain, however, unknown. Here, we have examined the relationship between galectin-7 and p53, a gene previously associated with upregulation of galectin-7. While RNA and protein analyses revealed a consistent and irreversible upregulation of galectin-7 throughout progression of lymphoma, no correlation with p53 was found. In fact, most of the lymphoma cell lines expressing high levels of galectin-7 did not express any detectable level of p53, although expressed
p21
Waf1/Cip1
gene following doxorubicin treatment, indicating that p53 was functional in these cells. Methylation-specific polymerase chain reaction (MS-PCR) analyses rather suggested that galectin-7 expression was associated with changes in DNA methylation. This conclusion was supported by data using demethylating agent 5-aza-dC. Furthermore, disruption of the DNA methylases
dnmt1 and
dnmt3a induced galectin-7. Collectively, our data suggest that abnormal expression of galectin-7 in lymphoma cells is not dependent on p53, but is rather associated with DNA hypomethylation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>19596268</pmid><doi>10.1016/j.bbrc.2009.07.015</doi><tpages>5</tpages></addata></record> |
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| subjects | Cell Line, Tumor Cyclin-Dependent Kinase Inhibitor p21 Cyclin-Dependent Kinase Inhibitor p21 - metabolism DNA (Cytosine-5-)-Methyltransferase DNA (Cytosine-5-)-Methyltransferase 1 DNA (Cytosine-5-)-Methyltransferases - genetics DNA (Cytosine-5-)-Methyltransferases - metabolism DNA Methylation Galectin-7 Galectins Galectins - genetics Gene Expression Gene Expression Regulation, Leukemic Human health and pathology Humans Infectious diseases Life Sciences Lymphoma Lymphoma - genetics p53 Promoter Regions, Genetic Tumor Suppressor Protein p53 Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism |
| title | Increased galectin-7 gene expression in lymphoma cells is under the control of DNA methylation |
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