TRAIP regulates Histone H2B monoubiquitination in DNA damage response pathways
Histone H2B monoubiquitination has been shown to play critical roles in diverse cellular processes including DNA damage response. Although recent data indicate that H2B monoubiquitination is strongly connected with tumor progression and regulation, the implications of this modification in lung adeno...
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| Veröffentlicht in: | Oncology reports 2019-06, Vol.41 (6), p.3305-3312 |
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| creator | Han, Ye Gi Yun, Miyong Choi, Minji Lee, Seok-Geun Kim, Hongtae |
| description | Histone H2B monoubiquitination has been shown to play critical roles in diverse cellular processes including DNA damage response. Although recent data indicate that H2B monoubiquitination is strongly connected with tumor progression and regulation, the implications of this modification in lung adenocarcinoma are relatively unknown. In the present study, we demonstrated the clinical implication of H2B monoubiquitination and the potential role of tumor necrosis factor receptor‑associated factor‑interacting protein (TRAIP) in regulating its modification in lung adenocarcinoma. Immunohistochemical analysis showed that H2B monoubiquitination was significantly downregulated in 68 human lung adenocarcinoma patient samples compared to their normal adjacent tissues. Depletion of TRAIP by specific siRNA treatment markedly decreased ionizing radiation (IR)‑induced H2B monoubiquitination. In addition, deletion mutants without RING domain or C‑terminus of TRAIP diminished the ability to induce H2B monoubiquitination at lysine 120. Notably, the nuclear expression of TRAIP was positively related with H2B monoubiquitination levels in patients with lung adenocarcinoma. Furthermore, statistical analysis indicated that low levels of both TRAIP and H2B monoubiquitination, not each alone, in patients with lung adenocarcinoma were strongly correlated with poor survival. Taken together, these results suggest that TRAIP is a novel regulator of H2B monoubiquitination in DNA damage response and cancer development in lung adenocarcinoma. |
| doi_str_mv | 10.3892/or.2019.7092 |
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Although recent data indicate that H2B monoubiquitination is strongly connected with tumor progression and regulation, the implications of this modification in lung adenocarcinoma are relatively unknown. In the present study, we demonstrated the clinical implication of H2B monoubiquitination and the potential role of tumor necrosis factor receptor‑associated factor‑interacting protein (TRAIP) in regulating its modification in lung adenocarcinoma. Immunohistochemical analysis showed that H2B monoubiquitination was significantly downregulated in 68 human lung adenocarcinoma patient samples compared to their normal adjacent tissues. Depletion of TRAIP by specific siRNA treatment markedly decreased ionizing radiation (IR)‑induced H2B monoubiquitination. In addition, deletion mutants without RING domain or C‑terminus of TRAIP diminished the ability to induce H2B monoubiquitination at lysine 120. Notably, the nuclear expression of TRAIP was positively related with H2B monoubiquitination levels in patients with lung adenocarcinoma. Furthermore, statistical analysis indicated that low levels of both TRAIP and H2B monoubiquitination, not each alone, in patients with lung adenocarcinoma were strongly correlated with poor survival. Taken together, these results suggest that TRAIP is a novel regulator of H2B monoubiquitination in DNA damage response and cancer development in lung adenocarcinoma.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2019.7092</identifier><identifier>PMID: 30942468</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Adenocarcinoma ; Cancer ; Cancer therapies ; Cell cycle ; Chemotherapy ; Cytotoxicity ; Deoxyribonucleic acid ; Development and progression ; DNA ; DNA damage ; DNA methylation ; DNA repair ; Enzymes ; Genetic aspects ; Health aspects ; Immunoglobulins ; Ionizing radiation ; Lung cancer ; Lysine ; Mutagenesis ; Necrosis ; Novels ; Patients ; Phosphorylation ; Physiological aspects ; Plasmids ; Proteins ; Radiation (Physics) ; Radiation therapy ; Recruitment ; Signal transduction ; Signaling peptides and proteins ; Tumor necrosis factor ; Tumor necrosis factor-TNF ; Tumors ; Ubiquitin-proteasome system</subject><ispartof>Oncology reports, 2019-06, Vol.41 (6), p.3305-3312</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-444f02096a56d6244ec4424a1f4809734d688fc30cd08fba8ec283a9def40b963</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30942468$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Han, Ye Gi</creatorcontrib><creatorcontrib>Yun, Miyong</creatorcontrib><creatorcontrib>Choi, Minji</creatorcontrib><creatorcontrib>Lee, Seok-Geun</creatorcontrib><creatorcontrib>Kim, Hongtae</creatorcontrib><title>TRAIP regulates Histone H2B monoubiquitination in DNA damage response pathways</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Histone H2B monoubiquitination has been shown to play critical roles in diverse cellular processes including DNA damage response. Although recent data indicate that H2B monoubiquitination is strongly connected with tumor progression and regulation, the implications of this modification in lung adenocarcinoma are relatively unknown. In the present study, we demonstrated the clinical implication of H2B monoubiquitination and the potential role of tumor necrosis factor receptor‑associated factor‑interacting protein (TRAIP) in regulating its modification in lung adenocarcinoma. Immunohistochemical analysis showed that H2B monoubiquitination was significantly downregulated in 68 human lung adenocarcinoma patient samples compared to their normal adjacent tissues. Depletion of TRAIP by specific siRNA treatment markedly decreased ionizing radiation (IR)‑induced H2B monoubiquitination. In addition, deletion mutants without RING domain or C‑terminus of TRAIP diminished the ability to induce H2B monoubiquitination at lysine 120. Notably, the nuclear expression of TRAIP was positively related with H2B monoubiquitination levels in patients with lung adenocarcinoma. Furthermore, statistical analysis indicated that low levels of both TRAIP and H2B monoubiquitination, not each alone, in patients with lung adenocarcinoma were strongly correlated with poor survival. Taken together, these results suggest that TRAIP is a novel regulator of H2B monoubiquitination in DNA damage response and cancer development in lung adenocarcinoma.</description><subject>Adenocarcinoma</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Chemotherapy</subject><subject>Cytotoxicity</subject><subject>Deoxyribonucleic acid</subject><subject>Development and progression</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA methylation</subject><subject>DNA repair</subject><subject>Enzymes</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Immunoglobulins</subject><subject>Ionizing radiation</subject><subject>Lung cancer</subject><subject>Lysine</subject><subject>Mutagenesis</subject><subject>Necrosis</subject><subject>Novels</subject><subject>Patients</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Plasmids</subject><subject>Proteins</subject><subject>Radiation (Physics)</subject><subject>Radiation therapy</subject><subject>Recruitment</subject><subject>Signal transduction</subject><subject>Signaling peptides and proteins</subject><subject>Tumor necrosis factor</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumors</subject><subject>Ubiquitin-proteasome system</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkd9KHDEUxkNR1G6963UZKJReONv8nUkut7a6gtRSLPQuZDPJbmQmWZMMxbfxWXyyZlBrLRJIDuH3fZxzPgDeIjgnXOBPIc4xRGLeQoFfgQPUClRjStBOqSFGNSHs1z54ndIVhLiFjdgD-wQKimnDD8DF5Y_F2fcqmvXYq2xStXQpB2_ubpf4czUEH8aVux5ddl5lF3zlfPXl26Lq1KDWpujSNvhkqq3Km9_qJr0Bu1b1yRw-vDPw8-Tr5fGyPr84PTtenNeaMpZrSqmFGIpGsaZrMKVG09KRQpZyKFpCu4ZzqwnUHeR2pbjRmBMlOmMpXImGzMDHe99tDNejSVkOLmnT98qbMCaJMcRNiyGlBX3_H3oVxuhLd4VCHDHEGHqi1qo30nkbclR6MpULxhlhhJd7BuYvUOV0ZnC67M268v9M8OEfwcaoPm9S6Mdpl-k5eHQP6hhSisbKbXSDijcSQTkFLUOUU9ByCrrg7x6GGleD6f7Cj8mSPxOuoAU</recordid><startdate>20190601</startdate><enddate>20190601</enddate><creator>Han, Ye Gi</creator><creator>Yun, Miyong</creator><creator>Choi, Minji</creator><creator>Lee, Seok-Geun</creator><creator>Kim, Hongtae</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><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>20190601</creationdate><title>TRAIP regulates Histone H2B monoubiquitination in DNA damage response pathways</title><author>Han, Ye Gi ; Yun, Miyong ; Choi, Minji ; Lee, Seok-Geun ; Kim, Hongtae</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-444f02096a56d6244ec4424a1f4809734d688fc30cd08fba8ec283a9def40b963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adenocarcinoma</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Chemotherapy</topic><topic>Cytotoxicity</topic><topic>Deoxyribonucleic acid</topic><topic>Development and progression</topic><topic>DNA</topic><topic>DNA damage</topic><topic>DNA methylation</topic><topic>DNA repair</topic><topic>Enzymes</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Immunoglobulins</topic><topic>Ionizing radiation</topic><topic>Lung cancer</topic><topic>Lysine</topic><topic>Mutagenesis</topic><topic>Necrosis</topic><topic>Novels</topic><topic>Patients</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Plasmids</topic><topic>Proteins</topic><topic>Radiation (Physics)</topic><topic>Radiation therapy</topic><topic>Recruitment</topic><topic>Signal transduction</topic><topic>Signaling peptides and proteins</topic><topic>Tumor necrosis factor</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumors</topic><topic>Ubiquitin-proteasome system</topic><toplevel>online_resources</toplevel><creatorcontrib>Han, Ye Gi</creatorcontrib><creatorcontrib>Yun, Miyong</creatorcontrib><creatorcontrib>Choi, Minji</creatorcontrib><creatorcontrib>Lee, Seok-Geun</creatorcontrib><creatorcontrib>Kim, Hongtae</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</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 Edition)</collection><collection>ProQuest Central UK/Ireland</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>Han, Ye Gi</au><au>Yun, Miyong</au><au>Choi, Minji</au><au>Lee, Seok-Geun</au><au>Kim, Hongtae</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TRAIP regulates Histone H2B monoubiquitination in DNA damage response pathways</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2019-06-01</date><risdate>2019</risdate><volume>41</volume><issue>6</issue><spage>3305</spage><epage>3312</epage><pages>3305-3312</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Histone H2B monoubiquitination has been shown to play critical roles in diverse cellular processes including DNA damage response. Although recent data indicate that H2B monoubiquitination is strongly connected with tumor progression and regulation, the implications of this modification in lung adenocarcinoma are relatively unknown. In the present study, we demonstrated the clinical implication of H2B monoubiquitination and the potential role of tumor necrosis factor receptor‑associated factor‑interacting protein (TRAIP) in regulating its modification in lung adenocarcinoma. Immunohistochemical analysis showed that H2B monoubiquitination was significantly downregulated in 68 human lung adenocarcinoma patient samples compared to their normal adjacent tissues. Depletion of TRAIP by specific siRNA treatment markedly decreased ionizing radiation (IR)‑induced H2B monoubiquitination. In addition, deletion mutants without RING domain or C‑terminus of TRAIP diminished the ability to induce H2B monoubiquitination at lysine 120. Notably, the nuclear expression of TRAIP was positively related with H2B monoubiquitination levels in patients with lung adenocarcinoma. Furthermore, statistical analysis indicated that low levels of both TRAIP and H2B monoubiquitination, not each alone, in patients with lung adenocarcinoma were strongly correlated with poor survival. Taken together, these results suggest that TRAIP is a novel regulator of H2B monoubiquitination in DNA damage response and cancer development in lung adenocarcinoma.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30942468</pmid><doi>10.3892/or.2019.7092</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma Cancer Cancer therapies Cell cycle Chemotherapy Cytotoxicity Deoxyribonucleic acid Development and progression DNA DNA damage DNA methylation DNA repair Enzymes Genetic aspects Health aspects Immunoglobulins Ionizing radiation Lung cancer Lysine Mutagenesis Necrosis Novels Patients Phosphorylation Physiological aspects Plasmids Proteins Radiation (Physics) Radiation therapy Recruitment Signal transduction Signaling peptides and proteins Tumor necrosis factor Tumor necrosis factor-TNF Tumors Ubiquitin-proteasome system |
| title | TRAIP regulates Histone H2B monoubiquitination in DNA damage response pathways |
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