Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma
The present study aimed to investigate the involvement of the Suv39H1 histone methyltransferase in the epigenetic changes in the euchromatic promoter in gastric carcinoma. We retrospectively analyzed the protein of Suv39H1 and tri-methylated histone H3 lysine 9 (H3K9) and histone H3 lysine 4 (H3K4)...
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description | The present study aimed to investigate the involvement of the Suv39H1 histone methyltransferase in the epigenetic changes in the euchromatic promoter in gastric carcinoma. We retrospectively analyzed the protein of Suv39H1 and tri-methylated histone H3 lysine 9 (H3K9) and histone H3 lysine 4 (H3K4) in 175 cases of gastric carcinoma by immunohistochemistry. Suv39H1 was depleted by siRNA, and cell apoptosis and cell proliferation were assessed by TUNEL and MTT assays, respectively. Histone methylated H3K9 and histone acetylated H3 and H4 were evaluated by western blotting. We found that the expression of Suv39H1 and tri-methylated H3K9 in gastric carcinoma was higher than that in benign gastric diseases (p0.05). Both Suv39H1 and tri-methylated H3K9 were positively correlated with the degree of differentiation, depth of infiltration and lymphatic invasion (p |
doi_str_mv | 10.3892/or.2014.3135 |
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We retrospectively analyzed the protein of Suv39H1 and tri-methylated histone H3 lysine 9 (H3K9) and histone H3 lysine 4 (H3K4) in 175 cases of gastric carcinoma by immunohistochemistry. Suv39H1 was depleted by siRNA, and cell apoptosis and cell proliferation were assessed by TUNEL and MTT assays, respectively. Histone methylated H3K9 and histone acetylated H3 and H4 were evaluated by western blotting. We found that the expression of Suv39H1 and tri-methylated H3K9 in gastric carcinoma was higher than that in benign gastric diseases (p<0.05). Tri-methylated H3K4 was similar in both tissue types (p>0.05). Both Suv39H1 and tri-methylated H3K9 were positively correlated with the degree of differentiation, depth of infiltration and lymphatic invasion (p<0.05) in gastric carcinoma. In addition, tri-methylated H3K9 was positively correlated with tumor stage, and node and metastatic statuses (p<0.05). Activation of Suv39H1 and overexpression of H3K9 tri-methylation may play an important role in tumorigenesis. They may be useful as a predictor for poor prognosis in gastric carcinoma. Silencing of the Suv39H1 gene decreased tri-methylated H3K9 and increased histone H3 acetylation, which caused activation of gene transcription, while there was no change in histone H4 acetylation. Depletion of Suv39H1 induced apoptosis and inhibited cell proliferation in the gastric cancer MGC803 cell line, while decreasing BCL-2, pro-caspase-9, pro-caspase-3 and C-myc. Suv39H1 may be a potential gene target for anti-gastric carcinoma therapy.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2014.3135</identifier><identifier>PMID: 24737085</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Aged ; Apoptosis ; Apoptosis - genetics ; Body mass index ; Caspase 3 - biosynthesis ; Cell growth ; Cell Proliferation - genetics ; Chromatin ; Deoxyribonucleic acid ; Development and progression ; DNA ; DNA methylation ; DNA Methylation - genetics ; Epigenesis, Genetic ; Epigenetics ; Female ; Gastric cancer ; gastric carcinoma ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genes ; Genetic aspects ; Health aspects ; histone methylation ; Histones - metabolism ; Humans ; Innovations ; Leukemia ; Male ; Metastasis ; Methyltransferases ; Methyltransferases - antagonists & inhibitors ; Methyltransferases - genetics ; Middle Aged ; Molecular targeted therapy ; Promoter Regions, Genetic ; Properties ; Protein expression ; Proteins ; Proto-Oncogene Proteins c-bcl-2 - biosynthesis ; Proto-Oncogene Proteins c-myc - biosynthesis ; Repressor Proteins - antagonists & inhibitors ; Repressor Proteins - genetics ; RNA, Small Interfering - genetics ; siRNA interference ; Stomach cancer ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology ; Suv39H1</subject><ispartof>Oncology reports, 2014-06, Vol.31 (6), p.2593-2600</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c552t-3346b6ba310b54e5372f69b381d3e0963eab70052a656265f050fa440f5149c63</citedby><cites>FETCH-LOGICAL-c552t-3346b6ba310b54e5372f69b381d3e0963eab70052a656265f050fa440f5149c63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24737085$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CAI, LISHENG</creatorcontrib><creatorcontrib>MA, XUDONG</creatorcontrib><creatorcontrib>HUANG, YIQUN</creatorcontrib><creatorcontrib>ZOU, YONG</creatorcontrib><creatorcontrib>CHEN, XINGSHENG</creatorcontrib><title>Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>The present study aimed to investigate the involvement of the Suv39H1 histone methyltransferase in the epigenetic changes in the euchromatic promoter in gastric carcinoma. We retrospectively analyzed the protein of Suv39H1 and tri-methylated histone H3 lysine 9 (H3K9) and histone H3 lysine 4 (H3K4) in 175 cases of gastric carcinoma by immunohistochemistry. Suv39H1 was depleted by siRNA, and cell apoptosis and cell proliferation were assessed by TUNEL and MTT assays, respectively. Histone methylated H3K9 and histone acetylated H3 and H4 were evaluated by western blotting. We found that the expression of Suv39H1 and tri-methylated H3K9 in gastric carcinoma was higher than that in benign gastric diseases (p<0.05). Tri-methylated H3K4 was similar in both tissue types (p>0.05). Both Suv39H1 and tri-methylated H3K9 were positively correlated with the degree of differentiation, depth of infiltration and lymphatic invasion (p<0.05) in gastric carcinoma. In addition, tri-methylated H3K9 was positively correlated with tumor stage, and node and metastatic statuses (p<0.05). Activation of Suv39H1 and overexpression of H3K9 tri-methylation may play an important role in tumorigenesis. They may be useful as a predictor for poor prognosis in gastric carcinoma. Silencing of the Suv39H1 gene decreased tri-methylated H3K9 and increased histone H3 acetylation, which caused activation of gene transcription, while there was no change in histone H4 acetylation. Depletion of Suv39H1 induced apoptosis and inhibited cell proliferation in the gastric cancer MGC803 cell line, while decreasing BCL-2, pro-caspase-9, pro-caspase-3 and C-myc. Suv39H1 may be a potential gene target for anti-gastric carcinoma therapy.</description><subject>Aged</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Body mass index</subject><subject>Caspase 3 - biosynthesis</subject><subject>Cell growth</subject><subject>Cell Proliferation - genetics</subject><subject>Chromatin</subject><subject>Deoxyribonucleic acid</subject><subject>Development and progression</subject><subject>DNA</subject><subject>DNA methylation</subject><subject>DNA Methylation - genetics</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetics</subject><subject>Female</subject><subject>Gastric cancer</subject><subject>gastric carcinoma</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>histone methylation</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>Innovations</subject><subject>Leukemia</subject><subject>Male</subject><subject>Metastasis</subject><subject>Methyltransferases</subject><subject>Methyltransferases - antagonists & inhibitors</subject><subject>Methyltransferases - genetics</subject><subject>Middle Aged</subject><subject>Molecular targeted therapy</subject><subject>Promoter Regions, Genetic</subject><subject>Properties</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-bcl-2 - biosynthesis</subject><subject>Proto-Oncogene Proteins c-myc - biosynthesis</subject><subject>Repressor Proteins - antagonists & inhibitors</subject><subject>Repressor Proteins - genetics</subject><subject>RNA, Small Interfering - genetics</subject><subject>siRNA interference</subject><subject>Stomach cancer</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><subject>Suv39H1</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkV2LFSEYgCWKdtu66zqEIPaiOamvOsfLw9K2wVL0Bd2J4-iOy8x4UifYf5_Dbqc2QkSR5_3wfRB6TskGtoq9iWnDCOUboCAeoGPaKtowDvRhvRNGGwDx_Qg9yfmaENYSqR6jI8ZbaMlWHKNPu86lZOaCh5BLnB2eXBluRlNCnLGZe1wGh533zhYcPf6y_AR1QXEOnz_scEWuTC4pWGxNsmGOk3mKHnkzZvfs7jxB387ffj27aC4_vnt_trtsrBCs1La47GRngJJOcCegZV6qDra0B0eUBGe6lhDBjBSSSeGJIN5wTrygXFkJJ-j0Nu8-xR-Ly0VPIVs3jmZ2ccmaCkaBcyCsoi__Qa_jkubanaYKmGyB1n2grszodJh9LMnYNaneccqYlFzySm3-Q9XVuynYOkAf6vu9gFd_BQzOjGXIcVzWAef74Otb0KaYc3Je71OYTLrRlOhVtY5Jr6r1qrriL-4-tXST6w_wb7d_Cud99Rj6mA9MTA3QhsiGCQXwC7WoquE</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>CAI, LISHENG</creator><creator>MA, XUDONG</creator><creator>HUANG, YIQUN</creator><creator>ZOU, YONG</creator><creator>CHEN, XINGSHENG</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20140601</creationdate><title>Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma</title><author>CAI, LISHENG ; MA, XUDONG ; HUANG, YIQUN ; ZOU, YONG ; CHEN, XINGSHENG</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c552t-3346b6ba310b54e5372f69b381d3e0963eab70052a656265f050fa440f5149c63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Aged</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Body mass index</topic><topic>Caspase 3 - biosynthesis</topic><topic>Cell growth</topic><topic>Cell Proliferation - genetics</topic><topic>Chromatin</topic><topic>Deoxyribonucleic acid</topic><topic>Development and progression</topic><topic>DNA</topic><topic>DNA methylation</topic><topic>DNA Methylation - genetics</topic><topic>Epigenesis, Genetic</topic><topic>Epigenetics</topic><topic>Female</topic><topic>Gastric cancer</topic><topic>gastric carcinoma</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>histone methylation</topic><topic>Histones - metabolism</topic><topic>Humans</topic><topic>Innovations</topic><topic>Leukemia</topic><topic>Male</topic><topic>Metastasis</topic><topic>Methyltransferases</topic><topic>Methyltransferases - antagonists & inhibitors</topic><topic>Methyltransferases - genetics</topic><topic>Middle Aged</topic><topic>Molecular targeted therapy</topic><topic>Promoter Regions, Genetic</topic><topic>Properties</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-bcl-2 - biosynthesis</topic><topic>Proto-Oncogene Proteins c-myc - biosynthesis</topic><topic>Repressor Proteins - antagonists & inhibitors</topic><topic>Repressor Proteins - genetics</topic><topic>RNA, Small Interfering - genetics</topic><topic>siRNA interference</topic><topic>Stomach cancer</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - pathology</topic><topic>Suv39H1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CAI, LISHENG</creatorcontrib><creatorcontrib>MA, XUDONG</creatorcontrib><creatorcontrib>HUANG, YIQUN</creatorcontrib><creatorcontrib>ZOU, YONG</creatorcontrib><creatorcontrib>CHEN, XINGSHENG</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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)</collection><collection>ProQuest Central</collection><collection>British Nursing Database</collection><collection>ProQuest Central</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>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CAI, LISHENG</au><au>MA, XUDONG</au><au>HUANG, YIQUN</au><au>ZOU, YONG</au><au>CHEN, XINGSHENG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>31</volume><issue>6</issue><spage>2593</spage><epage>2600</epage><pages>2593-2600</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>The present study aimed to investigate the involvement of the Suv39H1 histone methyltransferase in the epigenetic changes in the euchromatic promoter in gastric carcinoma. We retrospectively analyzed the protein of Suv39H1 and tri-methylated histone H3 lysine 9 (H3K9) and histone H3 lysine 4 (H3K4) in 175 cases of gastric carcinoma by immunohistochemistry. Suv39H1 was depleted by siRNA, and cell apoptosis and cell proliferation were assessed by TUNEL and MTT assays, respectively. Histone methylated H3K9 and histone acetylated H3 and H4 were evaluated by western blotting. We found that the expression of Suv39H1 and tri-methylated H3K9 in gastric carcinoma was higher than that in benign gastric diseases (p<0.05). Tri-methylated H3K4 was similar in both tissue types (p>0.05). Both Suv39H1 and tri-methylated H3K9 were positively correlated with the degree of differentiation, depth of infiltration and lymphatic invasion (p<0.05) in gastric carcinoma. In addition, tri-methylated H3K9 was positively correlated with tumor stage, and node and metastatic statuses (p<0.05). Activation of Suv39H1 and overexpression of H3K9 tri-methylation may play an important role in tumorigenesis. They may be useful as a predictor for poor prognosis in gastric carcinoma. Silencing of the Suv39H1 gene decreased tri-methylated H3K9 and increased histone H3 acetylation, which caused activation of gene transcription, while there was no change in histone H4 acetylation. Depletion of Suv39H1 induced apoptosis and inhibited cell proliferation in the gastric cancer MGC803 cell line, while decreasing BCL-2, pro-caspase-9, pro-caspase-3 and C-myc. Suv39H1 may be a potential gene target for anti-gastric carcinoma therapy.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>24737085</pmid><doi>10.3892/or.2014.3135</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aged Apoptosis Apoptosis - genetics Body mass index Caspase 3 - biosynthesis Cell growth Cell Proliferation - genetics Chromatin Deoxyribonucleic acid Development and progression DNA DNA methylation DNA Methylation - genetics Epigenesis, Genetic Epigenetics Female Gastric cancer gastric carcinoma Gene expression Gene Expression Regulation, Neoplastic Genes Genetic aspects Health aspects histone methylation Histones - metabolism Humans Innovations Leukemia Male Metastasis Methyltransferases Methyltransferases - antagonists & inhibitors Methyltransferases - genetics Middle Aged Molecular targeted therapy Promoter Regions, Genetic Properties Protein expression Proteins Proto-Oncogene Proteins c-bcl-2 - biosynthesis Proto-Oncogene Proteins c-myc - biosynthesis Repressor Proteins - antagonists & inhibitors Repressor Proteins - genetics RNA, Small Interfering - genetics siRNA interference Stomach cancer Stomach Neoplasms - genetics Stomach Neoplasms - pathology Suv39H1 |
title | Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma |
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