Up-regulation of dbpA mRNA in hepatocellular carcinoma associated with metabolic syndrome
Purpose Metabolic syndrome (MS) is a group of recognized risk factors for the development of hepatocellular carcinoma (HCC) in patients with chronic liver disease. The aim of this study was to analyze the clinicopathological characteristics of HCC patients with MS and the risk factors for recurrence...
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| Veröffentlicht in: | Hepatology international 2013-03, Vol.7 (1), p.215-225 |
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| creator | Obulhasim, Gulanbar Yasen, Mahmut Kajino, Kazunori Mogushi, Kaoru Tanaka, Shinji Mizushima, Hiroshi Tanaka, Hiroshi Arii, Shigeki Hino, Okio |
| description | Purpose
Metabolic syndrome (MS) is a group of recognized risk factors for the development of hepatocellular carcinoma (HCC) in patients with chronic liver disease. The aim of this study was to analyze the clinicopathological characteristics of HCC patients with MS and the risk factors for recurrence. Also, the aim was to investigate the cold shock protein: DNA-binding protein A (dbpA) expression in HCC patients with MS.
Methods
A total of 243 patients who underwent curative resections for HCC were classified into two groups. dbpA expression was investigated in 66 HCC patients with MS and in 30 patients without MS by using real-time RT-PCR. Promoter methylation status was examined by using MS-PCR.
Results
The incidence of metabolic factors affect the HCC significantly higher in non-B non-C patients than in hepatitis B virus (HBV) or hepatitis C virus (HCV) patients (
P
|
| doi_str_mv | 10.1007/s12072-012-9357-4 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1699489942</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1699489942</sourcerecordid><originalsourceid>FETCH-LOGICAL-c405t-cc5e8020183b5b1785f8ba5fcf03d92586b0f6de8acfa6fdc7ee042e58b11fa73</originalsourceid><addsrcrecordid>eNqFkU1r3DAQhkVpaD7aH5BLEPSSixuNZMnycQlJGwgthOyhJyHLo8TBthzJJuTfV8tulxAoPYgR6JlXMzyEnAL7BoxVFwk4q3jBgBe1kFVRfiBHUAtVMFnCx_1diENynNITY1IqUJ_IIVecgRLqiPxeT0XEh6W3cxdGGjxtm2lFh7ufK9qN9BEnOweHfZ-JSJ2NrhvDYKlNKbjOztjSl25-pAPOtgl952h6HdsYBvxMDrztE37Z1ROyvr66v_xR3P76fnO5ui1cyeRcOCdRszyOFo1soNLS68ZK7zwTbc2lVg3zqkVtnbfKt65CZCVHqRsAbytxQs63uVMMzwum2Qxd2kxsRwxLMqDqutT58P-jggsNFTCR0a_v0KewxDEvkimoVC1lXWYKtpSLIaWI3kyxG2x8NcDMRpHZKjJZkdkoMpues13y0gzY7jv-OskA3wIpP40PGN98_c_UP-aVm6M</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1317695594</pqid></control><display><type>article</type><title>Up-regulation of dbpA mRNA in hepatocellular carcinoma associated with metabolic syndrome</title><source>Springer Nature - Complete Springer Journals</source><creator>Obulhasim, Gulanbar ; Yasen, Mahmut ; Kajino, Kazunori ; Mogushi, Kaoru ; Tanaka, Shinji ; Mizushima, Hiroshi ; Tanaka, Hiroshi ; Arii, Shigeki ; Hino, Okio</creator><creatorcontrib>Obulhasim, Gulanbar ; Yasen, Mahmut ; Kajino, Kazunori ; Mogushi, Kaoru ; Tanaka, Shinji ; Mizushima, Hiroshi ; Tanaka, Hiroshi ; Arii, Shigeki ; Hino, Okio</creatorcontrib><description>Purpose
Metabolic syndrome (MS) is a group of recognized risk factors for the development of hepatocellular carcinoma (HCC) in patients with chronic liver disease. The aim of this study was to analyze the clinicopathological characteristics of HCC patients with MS and the risk factors for recurrence. Also, the aim was to investigate the cold shock protein: DNA-binding protein A (dbpA) expression in HCC patients with MS.
Methods
A total of 243 patients who underwent curative resections for HCC were classified into two groups. dbpA expression was investigated in 66 HCC patients with MS and in 30 patients without MS by using real-time RT-PCR. Promoter methylation status was examined by using MS-PCR.
Results
The incidence of metabolic factors affect the HCC significantly higher in non-B non-C patients than in hepatitis B virus (HBV) or hepatitis C virus (HCV) patients (
P
< 0.001). Univariate analysis of HCC patients with MS recurrence revealed aspartate amino transferase (AST), multiple tumors, liver damage, hepatic vein invasion, advanced cancer stages (
P
< 0.01), alpha-fetoprotein (AFP) and diabetes mellitus type II (
P
< 0.05) as risk factors. Multivariate analysis, AST, multiple tumors, and hepatic vein invasion (
P
< 0.01) were identified as independent factors for the recurrence. dbpA mRNA was higher in patients with MS than in those without MS (
P
= 0.016), and it was mostly upregulated in non-B non-C HCC patients with MS than in non-B non-C HCC patients without HBV or HCV. Especially, in HCC patients with diabetes mellitus type II, the mRNA and protein levels were highly upregulated. The dbpA expression was regulated by promoter methylation status (
P
< 0.05).
Conclusions
This study identifies that dbpA may accelerate the hepatocarcinogenesis in HCC patients with MS via inflammation-induced and oxidative stress pathways. The demethylation-related epigenetic activation may be one of the regulating factors for HCC patients with MS.</description><identifier>ISSN: 1936-0533</identifier><identifier>EISSN: 1936-0541</identifier><identifier>DOI: 10.1007/s12072-012-9357-4</identifier><identifier>PMID: 26201636</identifier><language>eng</language><publisher>India: Springer-Verlag</publisher><subject>alpha -fetoprotein ; Cold shock proteins ; Colorectal Surgery ; Diabetes mellitus ; DNA methylation ; DNA-binding protein ; epigenetics ; hepatic vein ; Hepatitis B virus ; Hepatitis C virus ; Hepatocellular carcinoma ; Hepatology ; Liver diseases ; Medicine ; Medicine & Public Health ; Metabolic disorders ; mRNA ; Multivariate analysis ; Original Article ; Oxidative stress ; Polymerase chain reaction ; Risk factors ; Surgery ; Tumors</subject><ispartof>Hepatology international, 2013-03, Vol.7 (1), p.215-225</ispartof><rights>Asian Pacific Association for the Study of the Liver 2012</rights><rights>Asian Pacific Association for the Study of the Liver 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-cc5e8020183b5b1785f8ba5fcf03d92586b0f6de8acfa6fdc7ee042e58b11fa73</citedby><cites>FETCH-LOGICAL-c405t-cc5e8020183b5b1785f8ba5fcf03d92586b0f6de8acfa6fdc7ee042e58b11fa73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12072-012-9357-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12072-012-9357-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26201636$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Obulhasim, Gulanbar</creatorcontrib><creatorcontrib>Yasen, Mahmut</creatorcontrib><creatorcontrib>Kajino, Kazunori</creatorcontrib><creatorcontrib>Mogushi, Kaoru</creatorcontrib><creatorcontrib>Tanaka, Shinji</creatorcontrib><creatorcontrib>Mizushima, Hiroshi</creatorcontrib><creatorcontrib>Tanaka, Hiroshi</creatorcontrib><creatorcontrib>Arii, Shigeki</creatorcontrib><creatorcontrib>Hino, Okio</creatorcontrib><title>Up-regulation of dbpA mRNA in hepatocellular carcinoma associated with metabolic syndrome</title><title>Hepatology international</title><addtitle>Hepatol Int</addtitle><addtitle>Hepatol Int</addtitle><description>Purpose
Metabolic syndrome (MS) is a group of recognized risk factors for the development of hepatocellular carcinoma (HCC) in patients with chronic liver disease. The aim of this study was to analyze the clinicopathological characteristics of HCC patients with MS and the risk factors for recurrence. Also, the aim was to investigate the cold shock protein: DNA-binding protein A (dbpA) expression in HCC patients with MS.
Methods
A total of 243 patients who underwent curative resections for HCC were classified into two groups. dbpA expression was investigated in 66 HCC patients with MS and in 30 patients without MS by using real-time RT-PCR. Promoter methylation status was examined by using MS-PCR.
Results
The incidence of metabolic factors affect the HCC significantly higher in non-B non-C patients than in hepatitis B virus (HBV) or hepatitis C virus (HCV) patients (
P
< 0.001). Univariate analysis of HCC patients with MS recurrence revealed aspartate amino transferase (AST), multiple tumors, liver damage, hepatic vein invasion, advanced cancer stages (
P
< 0.01), alpha-fetoprotein (AFP) and diabetes mellitus type II (
P
< 0.05) as risk factors. Multivariate analysis, AST, multiple tumors, and hepatic vein invasion (
P
< 0.01) were identified as independent factors for the recurrence. dbpA mRNA was higher in patients with MS than in those without MS (
P
= 0.016), and it was mostly upregulated in non-B non-C HCC patients with MS than in non-B non-C HCC patients without HBV or HCV. Especially, in HCC patients with diabetes mellitus type II, the mRNA and protein levels were highly upregulated. The dbpA expression was regulated by promoter methylation status (
P
< 0.05).
Conclusions
This study identifies that dbpA may accelerate the hepatocarcinogenesis in HCC patients with MS via inflammation-induced and oxidative stress pathways. The demethylation-related epigenetic activation may be one of the regulating factors for HCC patients with MS.</description><subject>alpha -fetoprotein</subject><subject>Cold shock proteins</subject><subject>Colorectal Surgery</subject><subject>Diabetes mellitus</subject><subject>DNA methylation</subject><subject>DNA-binding protein</subject><subject>epigenetics</subject><subject>hepatic vein</subject><subject>Hepatitis B virus</subject><subject>Hepatitis C virus</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatology</subject><subject>Liver diseases</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic disorders</subject><subject>mRNA</subject><subject>Multivariate analysis</subject><subject>Original Article</subject><subject>Oxidative stress</subject><subject>Polymerase chain reaction</subject><subject>Risk factors</subject><subject>Surgery</subject><subject>Tumors</subject><issn>1936-0533</issn><issn>1936-0541</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNqFkU1r3DAQhkVpaD7aH5BLEPSSixuNZMnycQlJGwgthOyhJyHLo8TBthzJJuTfV8tulxAoPYgR6JlXMzyEnAL7BoxVFwk4q3jBgBe1kFVRfiBHUAtVMFnCx_1diENynNITY1IqUJ_IIVecgRLqiPxeT0XEh6W3cxdGGjxtm2lFh7ufK9qN9BEnOweHfZ-JSJ2NrhvDYKlNKbjOztjSl25-pAPOtgl952h6HdsYBvxMDrztE37Z1ROyvr66v_xR3P76fnO5ui1cyeRcOCdRszyOFo1soNLS68ZK7zwTbc2lVg3zqkVtnbfKt65CZCVHqRsAbytxQs63uVMMzwum2Qxd2kxsRwxLMqDqutT58P-jggsNFTCR0a_v0KewxDEvkimoVC1lXWYKtpSLIaWI3kyxG2x8NcDMRpHZKjJZkdkoMpues13y0gzY7jv-OskA3wIpP40PGN98_c_UP-aVm6M</recordid><startdate>20130301</startdate><enddate>20130301</enddate><creator>Obulhasim, Gulanbar</creator><creator>Yasen, Mahmut</creator><creator>Kajino, Kazunori</creator><creator>Mogushi, Kaoru</creator><creator>Tanaka, Shinji</creator><creator>Mizushima, Hiroshi</creator><creator>Tanaka, Hiroshi</creator><creator>Arii, Shigeki</creator><creator>Hino, Okio</creator><general>Springer-Verlag</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7TM</scope><scope>7X8</scope></search><sort><creationdate>20130301</creationdate><title>Up-regulation of dbpA mRNA in hepatocellular carcinoma associated with metabolic syndrome</title><author>Obulhasim, Gulanbar ; Yasen, Mahmut ; Kajino, Kazunori ; Mogushi, Kaoru ; Tanaka, Shinji ; Mizushima, Hiroshi ; Tanaka, Hiroshi ; Arii, Shigeki ; Hino, Okio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-cc5e8020183b5b1785f8ba5fcf03d92586b0f6de8acfa6fdc7ee042e58b11fa73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>alpha -fetoprotein</topic><topic>Cold shock proteins</topic><topic>Colorectal Surgery</topic><topic>Diabetes mellitus</topic><topic>DNA methylation</topic><topic>DNA-binding protein</topic><topic>epigenetics</topic><topic>hepatic vein</topic><topic>Hepatitis B virus</topic><topic>Hepatitis C virus</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatology</topic><topic>Liver diseases</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic disorders</topic><topic>mRNA</topic><topic>Multivariate analysis</topic><topic>Original Article</topic><topic>Oxidative stress</topic><topic>Polymerase chain reaction</topic><topic>Risk factors</topic><topic>Surgery</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Obulhasim, Gulanbar</creatorcontrib><creatorcontrib>Yasen, Mahmut</creatorcontrib><creatorcontrib>Kajino, Kazunori</creatorcontrib><creatorcontrib>Mogushi, Kaoru</creatorcontrib><creatorcontrib>Tanaka, Shinji</creatorcontrib><creatorcontrib>Mizushima, Hiroshi</creatorcontrib><creatorcontrib>Tanaka, Hiroshi</creatorcontrib><creatorcontrib>Arii, Shigeki</creatorcontrib><creatorcontrib>Hino, Okio</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Proquest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Nucleic Acids Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Hepatology international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Obulhasim, Gulanbar</au><au>Yasen, Mahmut</au><au>Kajino, Kazunori</au><au>Mogushi, Kaoru</au><au>Tanaka, Shinji</au><au>Mizushima, Hiroshi</au><au>Tanaka, Hiroshi</au><au>Arii, Shigeki</au><au>Hino, Okio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Up-regulation of dbpA mRNA in hepatocellular carcinoma associated with metabolic syndrome</atitle><jtitle>Hepatology international</jtitle><stitle>Hepatol Int</stitle><addtitle>Hepatol Int</addtitle><date>2013-03-01</date><risdate>2013</risdate><volume>7</volume><issue>1</issue><spage>215</spage><epage>225</epage><pages>215-225</pages><issn>1936-0533</issn><eissn>1936-0541</eissn><abstract>Purpose
Metabolic syndrome (MS) is a group of recognized risk factors for the development of hepatocellular carcinoma (HCC) in patients with chronic liver disease. The aim of this study was to analyze the clinicopathological characteristics of HCC patients with MS and the risk factors for recurrence. Also, the aim was to investigate the cold shock protein: DNA-binding protein A (dbpA) expression in HCC patients with MS.
Methods
A total of 243 patients who underwent curative resections for HCC were classified into two groups. dbpA expression was investigated in 66 HCC patients with MS and in 30 patients without MS by using real-time RT-PCR. Promoter methylation status was examined by using MS-PCR.
Results
The incidence of metabolic factors affect the HCC significantly higher in non-B non-C patients than in hepatitis B virus (HBV) or hepatitis C virus (HCV) patients (
P
< 0.001). Univariate analysis of HCC patients with MS recurrence revealed aspartate amino transferase (AST), multiple tumors, liver damage, hepatic vein invasion, advanced cancer stages (
P
< 0.01), alpha-fetoprotein (AFP) and diabetes mellitus type II (
P
< 0.05) as risk factors. Multivariate analysis, AST, multiple tumors, and hepatic vein invasion (
P
< 0.01) were identified as independent factors for the recurrence. dbpA mRNA was higher in patients with MS than in those without MS (
P
= 0.016), and it was mostly upregulated in non-B non-C HCC patients with MS than in non-B non-C HCC patients without HBV or HCV. Especially, in HCC patients with diabetes mellitus type II, the mRNA and protein levels were highly upregulated. The dbpA expression was regulated by promoter methylation status (
P
< 0.05).
Conclusions
This study identifies that dbpA may accelerate the hepatocarcinogenesis in HCC patients with MS via inflammation-induced and oxidative stress pathways. The demethylation-related epigenetic activation may be one of the regulating factors for HCC patients with MS.</abstract><cop>India</cop><pub>Springer-Verlag</pub><pmid>26201636</pmid><doi>10.1007/s12072-012-9357-4</doi><tpages>11</tpages></addata></record> |
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| ispartof | Hepatology international, 2013-03, Vol.7 (1), p.215-225 |
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| language | eng |
| recordid | cdi_proquest_miscellaneous_1699489942 |
| source | Springer Nature - Complete Springer Journals |
| subjects | alpha -fetoprotein Cold shock proteins Colorectal Surgery Diabetes mellitus DNA methylation DNA-binding protein epigenetics hepatic vein Hepatitis B virus Hepatitis C virus Hepatocellular carcinoma Hepatology Liver diseases Medicine Medicine & Public Health Metabolic disorders mRNA Multivariate analysis Original Article Oxidative stress Polymerase chain reaction Risk factors Surgery Tumors |
| title | Up-regulation of dbpA mRNA in hepatocellular carcinoma associated with metabolic syndrome |
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