DNA hypermethylation at the D17S5 locus and reduced HIC-1 mRNA expression are associated with hepatocarcinogenesis
To examine the significance of aberrant DNA methylation in hepatocarcinogenesis, the DNA methylation status at the D17S5 locus and mRNA expression of a candidate tumor suppressor gene, HIC-1 (hypermethylated-in-cancer), which was identified at the D17S5 locus, in primary hepatocellular carcinomas (H...
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| Veröffentlicht in: | Hepatology (Baltimore, Md.) Md.), 1999-03, Vol.29 (3), p.703-709 |
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| container_title | Hepatology (Baltimore, Md.) |
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| creator | KANAI, Y HUI, A.-M LIN SUN USHIJIMA, S SAKAMOTO, M TSUDA, H HIROHASHI, S |
| description | To examine the significance of aberrant DNA methylation in hepatocarcinogenesis, the DNA methylation status at the D17S5 locus and mRNA expression of a candidate tumor suppressor gene, HIC-1 (hypermethylated-in-cancer), which was identified at the D17S5 locus, in primary hepatocellular carcinomas (HCCs) and their corresponding noncancerous liver tissues were assessed. DNA hypermethylation at the D17S5 locus was detected in 44% of the noncancerous liver tissues showing chronic hepatitis or cirrhosis, which are widely considered to be precancerous conditions, but was not observed in noncancerous liver tissues showing no remarkable histological findings. The incidence of DNA hypermethylation at this locus was significantly higher in HCCs (90%) than noncancerous liver tissues (P |
| doi_str_mv | 10.1002/hep.510290338 |
| format | Article |
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DNA hypermethylation at the D17S5 locus was detected in 44% of the noncancerous liver tissues showing chronic hepatitis or cirrhosis, which are widely considered to be precancerous conditions, but was not observed in noncancerous liver tissues showing no remarkable histological findings. The incidence of DNA hypermethylation at this locus was significantly higher in HCCs (90%) than noncancerous liver tissues (P <.001). Loss of heterozygosity at the D17S5 locus, which was preceded by DNA hypermethylation at the same locus, was detected in 54% of HCCs. The HIC-1 mRNA expression level of noncancerous liver tissues showing chronic hepatitis or cirrhosis was significantly lower than that of noncancerous liver tissues showing no remarkable histological findings (P <.01), and that of HCCs was even lower than that of noncancerous liver tissues (P <.05). Poorly differentiated HCCs showed lower expression levels than well- to moderately differentiated HCCs. Mutation of the p53 gene may be involved in HIC-1 inactivation. Moreover, wild-type p53 did not overcome DNA hypermethylation at the D17S5 locus to activate HIC-1 in HCCs. These data suggest that aberrant DNA methylation at this locus and reduced HIC-1 mRNA expression participate in hepatocarcinogenesis during both early developmental stages and malignant progression of HCCs.</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.510290338</identifier><identifier>PMID: 10051471</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>Hoboken, NJ: Wiley</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - metabolism ; Chromosome Mapping ; DNA - genetics ; DNA - metabolism ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Kruppel-Like Transcription Factors ; Liver - metabolism ; Liver Neoplasms - genetics ; Liver Neoplasms - metabolism ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Loss of Heterozygosity ; Male ; Medical sciences ; Methylation ; Middle Aged ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Transcription Factors - genetics ; Tumors</subject><ispartof>Hepatology (Baltimore, Md.), 1999-03, Vol.29 (3), p.703-709</ispartof><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c274t-d31ce22961045a843228111e4a0debc21bb00ecd9a7b0322fec223b558135e2e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1705211$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10051471$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KANAI, Y</creatorcontrib><creatorcontrib>HUI, A.-M</creatorcontrib><creatorcontrib>LIN SUN</creatorcontrib><creatorcontrib>USHIJIMA, S</creatorcontrib><creatorcontrib>SAKAMOTO, M</creatorcontrib><creatorcontrib>TSUDA, H</creatorcontrib><creatorcontrib>HIROHASHI, S</creatorcontrib><title>DNA hypermethylation at the D17S5 locus and reduced HIC-1 mRNA expression are associated with hepatocarcinogenesis</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>To examine the significance of aberrant DNA methylation in hepatocarcinogenesis, the DNA methylation status at the D17S5 locus and mRNA expression of a candidate tumor suppressor gene, HIC-1 (hypermethylated-in-cancer), which was identified at the D17S5 locus, in primary hepatocellular carcinomas (HCCs) and their corresponding noncancerous liver tissues were assessed. DNA hypermethylation at the D17S5 locus was detected in 44% of the noncancerous liver tissues showing chronic hepatitis or cirrhosis, which are widely considered to be precancerous conditions, but was not observed in noncancerous liver tissues showing no remarkable histological findings. The incidence of DNA hypermethylation at this locus was significantly higher in HCCs (90%) than noncancerous liver tissues (P <.001). Loss of heterozygosity at the D17S5 locus, which was preceded by DNA hypermethylation at the same locus, was detected in 54% of HCCs. The HIC-1 mRNA expression level of noncancerous liver tissues showing chronic hepatitis or cirrhosis was significantly lower than that of noncancerous liver tissues showing no remarkable histological findings (P <.01), and that of HCCs was even lower than that of noncancerous liver tissues (P <.05). Poorly differentiated HCCs showed lower expression levels than well- to moderately differentiated HCCs. Mutation of the p53 gene may be involved in HIC-1 inactivation. Moreover, wild-type p53 did not overcome DNA hypermethylation at the D17S5 locus to activate HIC-1 in HCCs. These data suggest that aberrant DNA methylation at this locus and reduced HIC-1 mRNA expression participate in hepatocarcinogenesis during both early developmental stages and malignant progression of HCCs.</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Chromosome Mapping</subject><subject>DNA - genetics</subject><subject>DNA - metabolism</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Kruppel-Like Transcription Factors</subject><subject>Liver - metabolism</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Loss of Heterozygosity</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Methylation</subject><subject>Middle Aged</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Transcription Factors - genetics</subject><subject>Tumors</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpN0E1P3DAQBmALtYItcOSKfKi4hc7Y8SY5ogUKEgKJj3PkOLMkKF_1OCr77zHdVduTD_O8o_ErxAnCOQKoHw1N5wZBFaB1vicWaFSWaG3gi1iAyiApUBcH4hvzGwAUqcr3xUFMGkwzXAh_eX8hm81EvqfQbDob2nGQNsjQkLzE7MnIbnQzSzvU0lM9O6rlze0qQdk_xii9T56Y_4Q8Scs8utaGiH63oZHxOhtGZ71rh_GVBuKWj8TXte2YjnfvoXi5vnpe3SR3Dz9vVxd3iVNZGpJaoyOliiVCamyeaqVyRKTUQk2VU1hVAOTqwmYVxOGanFK6MiZHbUiRPhRn272TH3_NxKHsW3bUdXagceZyWSwBsyVEmGyh8yOzp3U5-ba3flMilJ8ll_Eb5d-Soz_dLZ6rnur_9LbVCL7vgGVnu7W3g2v5n8vAKET9AeYBg80</recordid><startdate>19990301</startdate><enddate>19990301</enddate><creator>KANAI, Y</creator><creator>HUI, A.-M</creator><creator>LIN SUN</creator><creator>USHIJIMA, S</creator><creator>SAKAMOTO, M</creator><creator>TSUDA, H</creator><creator>HIROHASHI, S</creator><general>Wiley</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>19990301</creationdate><title>DNA hypermethylation at the D17S5 locus and reduced HIC-1 mRNA expression are associated with hepatocarcinogenesis</title><author>KANAI, Y ; HUI, A.-M ; LIN SUN ; USHIJIMA, S ; SAKAMOTO, M ; TSUDA, H ; HIROHASHI, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c274t-d31ce22961045a843228111e4a0debc21bb00ecd9a7b0322fec223b558135e2e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Chromosome Mapping</topic><topic>DNA - genetics</topic><topic>DNA - metabolism</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Kruppel-Like Transcription Factors</topic><topic>Liver - metabolism</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Loss of Heterozygosity</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Methylation</topic><topic>Middle Aged</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Transcription Factors - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KANAI, Y</creatorcontrib><creatorcontrib>HUI, A.-M</creatorcontrib><creatorcontrib>LIN SUN</creatorcontrib><creatorcontrib>USHIJIMA, S</creatorcontrib><creatorcontrib>SAKAMOTO, M</creatorcontrib><creatorcontrib>TSUDA, H</creatorcontrib><creatorcontrib>HIROHASHI, S</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KANAI, Y</au><au>HUI, A.-M</au><au>LIN SUN</au><au>USHIJIMA, S</au><au>SAKAMOTO, M</au><au>TSUDA, H</au><au>HIROHASHI, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DNA hypermethylation at the D17S5 locus and reduced HIC-1 mRNA expression are associated with hepatocarcinogenesis</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>1999-03-01</date><risdate>1999</risdate><volume>29</volume><issue>3</issue><spage>703</spage><epage>709</epage><pages>703-709</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><coden>HPTLD9</coden><abstract>To examine the significance of aberrant DNA methylation in hepatocarcinogenesis, the DNA methylation status at the D17S5 locus and mRNA expression of a candidate tumor suppressor gene, HIC-1 (hypermethylated-in-cancer), which was identified at the D17S5 locus, in primary hepatocellular carcinomas (HCCs) and their corresponding noncancerous liver tissues were assessed. DNA hypermethylation at the D17S5 locus was detected in 44% of the noncancerous liver tissues showing chronic hepatitis or cirrhosis, which are widely considered to be precancerous conditions, but was not observed in noncancerous liver tissues showing no remarkable histological findings. The incidence of DNA hypermethylation at this locus was significantly higher in HCCs (90%) than noncancerous liver tissues (P <.001). Loss of heterozygosity at the D17S5 locus, which was preceded by DNA hypermethylation at the same locus, was detected in 54% of HCCs. The HIC-1 mRNA expression level of noncancerous liver tissues showing chronic hepatitis or cirrhosis was significantly lower than that of noncancerous liver tissues showing no remarkable histological findings (P <.01), and that of HCCs was even lower than that of noncancerous liver tissues (P <.05). Poorly differentiated HCCs showed lower expression levels than well- to moderately differentiated HCCs. Mutation of the p53 gene may be involved in HIC-1 inactivation. Moreover, wild-type p53 did not overcome DNA hypermethylation at the D17S5 locus to activate HIC-1 in HCCs. These data suggest that aberrant DNA methylation at this locus and reduced HIC-1 mRNA expression participate in hepatocarcinogenesis during both early developmental stages and malignant progression of HCCs.</abstract><cop>Hoboken, NJ</cop><pub>Wiley</pub><pmid>10051471</pmid><doi>10.1002/hep.510290338</doi><tpages>7</tpages></addata></record> |
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| subjects | Adult Aged Biological and medical sciences Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - metabolism Chromosome Mapping DNA - genetics DNA - metabolism Female Gastroenterology. Liver. Pancreas. Abdomen Humans Kruppel-Like Transcription Factors Liver - metabolism Liver Neoplasms - genetics Liver Neoplasms - metabolism Liver. Biliary tract. Portal circulation. Exocrine pancreas Loss of Heterozygosity Male Medical sciences Methylation Middle Aged Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Transcription Factors - genetics Tumors |
| title | DNA hypermethylation at the D17S5 locus and reduced HIC-1 mRNA expression are associated with hepatocarcinogenesis |
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