Elevated Expression of Hepatoma Up-Regulated Protein Inhibits γ-Irradiation-Induced Apoptosis of Prostate Cancer Cells
ABSTRACT Despite progression in diagnosis and treatment, prostate cancer (PCa) still represents the main cause of cancer‐related mortality and morbidity in men. Although radiation therapy offers clinical benefit over other therapeutic modalities, the success of this therapeutic modality is commonly...
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| Veröffentlicht in: | Journal of cellular biochemistry 2016-06, Vol.117 (6), p.1308-1318 |
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| creator | Hassan, Mohamed El Khattouti, Abdelouahid Ejaeidi, Ahmed Ma, Tangeng Day, William A. Espinoza, Ingrid Vijayakumar, Srinivasan Gomez, Christian R. |
| description | ABSTRACT
Despite progression in diagnosis and treatment, prostate cancer (PCa) still represents the main cause of cancer‐related mortality and morbidity in men. Although radiation therapy offers clinical benefit over other therapeutic modalities, the success of this therapeutic modality is commonly hampered by the resistance of advanced tumors. So far, the mechanisms governing tumor resistance to radiotherapy are not discussed in detail. Here, we demonstrate for the first time that the resistance of PCa to radiation therapy is attributed to elevated expression of Hepatoma Up‐Regulated Protein (HURP). In PCa cells, the induction of HURP expression suppresses γ‐irradiation‐induced apoptosis. γ‐irradiation‐induced apoptosis of PCa cells is associated with expression of E2F1, p53, p21 proteins together with the phosphorylation of apoptosis signal‐regulating kinase1 (ASK1), c‐jun‐N‐terminal kinase (JNK) and Ataxia‐telangiectasia mutated (ATM) and histone family member X (H2AX). Whereas, the induction of HURP expression is able to suppress γ‐irradiation‐induced effects on E2F1, p53, p21, ATM, ASK1, JNK and ATM, and H2AX. Also, inhibition of γ‐irradiation‐induced‐ cytochrome c release, cleavage of caspase‐9, caspase‐3, PARP, and reactive oxygen species (ROS) were noted in PCa cells induced for HURP expression. The observed radio‐resistance of PCa is thought to be the consequence of HURP‐mediated destabilization of p53 and ATM proteins that are essential for the modulation of γ‐irradiation‐induced apoptosis. Thus, based on our findings, PCa resistance to radiation therapy results from the deregulation of ASK1/ JNK; ATM/ H2AX; ATM/p53 and checkpoint kinase 2 (Chk2)/ E2F‐1 in response to the elevated expression of HURP. J. Cell. Biochem. 117: 1308–1318, 2016. © 2015 Wiley Periodicals, Inc. |
| doi_str_mv | 10.1002/jcb.25419 |
| format | Article |
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Despite progression in diagnosis and treatment, prostate cancer (PCa) still represents the main cause of cancer‐related mortality and morbidity in men. Although radiation therapy offers clinical benefit over other therapeutic modalities, the success of this therapeutic modality is commonly hampered by the resistance of advanced tumors. So far, the mechanisms governing tumor resistance to radiotherapy are not discussed in detail. Here, we demonstrate for the first time that the resistance of PCa to radiation therapy is attributed to elevated expression of Hepatoma Up‐Regulated Protein (HURP). In PCa cells, the induction of HURP expression suppresses γ‐irradiation‐induced apoptosis. γ‐irradiation‐induced apoptosis of PCa cells is associated with expression of E2F1, p53, p21 proteins together with the phosphorylation of apoptosis signal‐regulating kinase1 (ASK1), c‐jun‐N‐terminal kinase (JNK) and Ataxia‐telangiectasia mutated (ATM) and histone family member X (H2AX). Whereas, the induction of HURP expression is able to suppress γ‐irradiation‐induced effects on E2F1, p53, p21, ATM, ASK1, JNK and ATM, and H2AX. Also, inhibition of γ‐irradiation‐induced‐ cytochrome c release, cleavage of caspase‐9, caspase‐3, PARP, and reactive oxygen species (ROS) were noted in PCa cells induced for HURP expression. The observed radio‐resistance of PCa is thought to be the consequence of HURP‐mediated destabilization of p53 and ATM proteins that are essential for the modulation of γ‐irradiation‐induced apoptosis. Thus, based on our findings, PCa resistance to radiation therapy results from the deregulation of ASK1/ JNK; ATM/ H2AX; ATM/p53 and checkpoint kinase 2 (Chk2)/ E2F‐1 in response to the elevated expression of HURP. J. Cell. Biochem. 117: 1308–1318, 2016. © 2015 Wiley Periodicals, Inc.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.25419</identifier><identifier>PMID: 26505164</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>APOPTOSIS ; ASK1 ; Ataxia ; Ataxia telangiectasia ; Ataxia telangiectasia mutated protein ; Ataxia Telangiectasia Mutated Proteins - metabolism ; Cancer therapies ; Caspase ; Cell Line, Tumor ; CHK2 protein ; Cyclin-dependent kinase inhibitor p21 ; Cytochrome c ; Cytochromes ; Deregulation ; Destabilization ; E2F1 protein ; Gamma Rays ; Gene Expression Regulation, Neoplastic ; Hepatoma ; Histone H2A ; Humans ; HURP ; Irradiation ; JNK ; JNK protein ; Kinases ; Liver cancer ; Male ; MAP kinase ; Morbidity ; Neoplasm Proteins - metabolism ; p53 Protein ; PCa ; Phosphorylation ; Poly(ADP-ribose) polymerase ; Prostate cancer ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - radiotherapy ; Proteins ; Radiation therapy ; Radiation Tolerance ; Reactive oxygen species ; Signal Transduction - radiation effects ; Tumor Suppressor Protein p53 - metabolism ; Tumors ; Ubiquitination ; Up-Regulation ; γ-IRRADIATION</subject><ispartof>Journal of cellular biochemistry, 2016-06, Vol.117 (6), p.1308-1318</ispartof><rights>2015 Wiley Periodicals, Inc.</rights><rights>2016 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3919-4b2e3c570e60159600fbd96c55472f7ae737fae84bb3994c742433aef4c951ba3</citedby><cites>FETCH-LOGICAL-c3919-4b2e3c570e60159600fbd96c55472f7ae737fae84bb3994c742433aef4c951ba3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.25419$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.25419$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26505164$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hassan, Mohamed</creatorcontrib><creatorcontrib>El Khattouti, Abdelouahid</creatorcontrib><creatorcontrib>Ejaeidi, Ahmed</creatorcontrib><creatorcontrib>Ma, Tangeng</creatorcontrib><creatorcontrib>Day, William A.</creatorcontrib><creatorcontrib>Espinoza, Ingrid</creatorcontrib><creatorcontrib>Vijayakumar, Srinivasan</creatorcontrib><creatorcontrib>Gomez, Christian R.</creatorcontrib><title>Elevated Expression of Hepatoma Up-Regulated Protein Inhibits γ-Irradiation-Induced Apoptosis of Prostate Cancer Cells</title><title>Journal of cellular biochemistry</title><addtitle>J. Cell. Biochem.</addtitle><description>ABSTRACT
Despite progression in diagnosis and treatment, prostate cancer (PCa) still represents the main cause of cancer‐related mortality and morbidity in men. Although radiation therapy offers clinical benefit over other therapeutic modalities, the success of this therapeutic modality is commonly hampered by the resistance of advanced tumors. So far, the mechanisms governing tumor resistance to radiotherapy are not discussed in detail. Here, we demonstrate for the first time that the resistance of PCa to radiation therapy is attributed to elevated expression of Hepatoma Up‐Regulated Protein (HURP). In PCa cells, the induction of HURP expression suppresses γ‐irradiation‐induced apoptosis. γ‐irradiation‐induced apoptosis of PCa cells is associated with expression of E2F1, p53, p21 proteins together with the phosphorylation of apoptosis signal‐regulating kinase1 (ASK1), c‐jun‐N‐terminal kinase (JNK) and Ataxia‐telangiectasia mutated (ATM) and histone family member X (H2AX). Whereas, the induction of HURP expression is able to suppress γ‐irradiation‐induced effects on E2F1, p53, p21, ATM, ASK1, JNK and ATM, and H2AX. Also, inhibition of γ‐irradiation‐induced‐ cytochrome c release, cleavage of caspase‐9, caspase‐3, PARP, and reactive oxygen species (ROS) were noted in PCa cells induced for HURP expression. The observed radio‐resistance of PCa is thought to be the consequence of HURP‐mediated destabilization of p53 and ATM proteins that are essential for the modulation of γ‐irradiation‐induced apoptosis. Thus, based on our findings, PCa resistance to radiation therapy results from the deregulation of ASK1/ JNK; ATM/ H2AX; ATM/p53 and checkpoint kinase 2 (Chk2)/ E2F‐1 in response to the elevated expression of HURP. J. Cell. Biochem. 117: 1308–1318, 2016. © 2015 Wiley Periodicals, Inc.</description><subject>APOPTOSIS</subject><subject>ASK1</subject><subject>Ataxia</subject><subject>Ataxia telangiectasia</subject><subject>Ataxia telangiectasia mutated protein</subject><subject>Ataxia Telangiectasia Mutated Proteins - metabolism</subject><subject>Cancer therapies</subject><subject>Caspase</subject><subject>Cell Line, Tumor</subject><subject>CHK2 protein</subject><subject>Cyclin-dependent kinase inhibitor p21</subject><subject>Cytochrome c</subject><subject>Cytochromes</subject><subject>Deregulation</subject><subject>Destabilization</subject><subject>E2F1 protein</subject><subject>Gamma Rays</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Hepatoma</subject><subject>Histone H2A</subject><subject>Humans</subject><subject>HURP</subject><subject>Irradiation</subject><subject>JNK</subject><subject>JNK protein</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>Male</subject><subject>MAP kinase</subject><subject>Morbidity</subject><subject>Neoplasm Proteins - metabolism</subject><subject>p53 Protein</subject><subject>PCa</subject><subject>Phosphorylation</subject><subject>Poly(ADP-ribose) polymerase</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - radiotherapy</subject><subject>Proteins</subject><subject>Radiation therapy</subject><subject>Radiation Tolerance</subject><subject>Reactive oxygen species</subject><subject>Signal Transduction - radiation effects</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumors</subject><subject>Ubiquitination</subject><subject>Up-Regulation</subject><subject>γ-IRRADIATION</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1u1DAUhS1ERYfCghdAkdjAwq1_4_GyRNPOVAWqioLExnKcG_CQiVM7oe1z8R48E26n7QKJlTff-XSuD0KvKNmnhLCDtav3mRRUP0EzSrTCohTiKZoRxQlmnLJd9DylNSFEa86eoV1WSiJpKWboatHBLztCUyyuhwgp-dAXoS2WMNgxbGxxMeBz-D51d8xZDCP4vlj1P3ztx1T8-Y1XMdrG2zEH8apvJpe5wyEMY0g-3apyKI05XlS2dxCLCrouvUA7re0SvLx_99DF0eJztcSnn45X1eEpdlxTjUXNgDupCJSESl0S0taNLp2UQrFWWVBctRbmoq651sIpwQTnFlrhtKS15Xvo7dY7xHA5QRrNxieXG9gewpQMVUoTJgRjGX3zD7oOU-xzO8MknXOiSsUz9W5LuXxWitCaIfqNjTeGEnO7hslrmLs1Mvv63jjVG2geyYfvz8DBFrjyHdz832ROqvcPSrxN-DTC9WPCxp8mt1PSfP14bObLb-cfzrLgC_8LOMOjKw</recordid><startdate>201606</startdate><enddate>201606</enddate><creator>Hassan, Mohamed</creator><creator>El Khattouti, Abdelouahid</creator><creator>Ejaeidi, Ahmed</creator><creator>Ma, Tangeng</creator><creator>Day, William A.</creator><creator>Espinoza, Ingrid</creator><creator>Vijayakumar, Srinivasan</creator><creator>Gomez, Christian R.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201606</creationdate><title>Elevated Expression of Hepatoma Up-Regulated Protein Inhibits γ-Irradiation-Induced Apoptosis of Prostate Cancer Cells</title><author>Hassan, Mohamed ; El Khattouti, Abdelouahid ; Ejaeidi, Ahmed ; Ma, Tangeng ; Day, William A. ; Espinoza, Ingrid ; Vijayakumar, Srinivasan ; Gomez, Christian R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3919-4b2e3c570e60159600fbd96c55472f7ae737fae84bb3994c742433aef4c951ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>APOPTOSIS</topic><topic>ASK1</topic><topic>Ataxia</topic><topic>Ataxia telangiectasia</topic><topic>Ataxia telangiectasia mutated protein</topic><topic>Ataxia Telangiectasia Mutated Proteins - metabolism</topic><topic>Cancer therapies</topic><topic>Caspase</topic><topic>Cell Line, Tumor</topic><topic>CHK2 protein</topic><topic>Cyclin-dependent kinase inhibitor p21</topic><topic>Cytochrome c</topic><topic>Cytochromes</topic><topic>Deregulation</topic><topic>Destabilization</topic><topic>E2F1 protein</topic><topic>Gamma Rays</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Hepatoma</topic><topic>Histone H2A</topic><topic>Humans</topic><topic>HURP</topic><topic>Irradiation</topic><topic>JNK</topic><topic>JNK protein</topic><topic>Kinases</topic><topic>Liver cancer</topic><topic>Male</topic><topic>MAP kinase</topic><topic>Morbidity</topic><topic>Neoplasm Proteins - metabolism</topic><topic>p53 Protein</topic><topic>PCa</topic><topic>Phosphorylation</topic><topic>Poly(ADP-ribose) polymerase</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - radiotherapy</topic><topic>Proteins</topic><topic>Radiation therapy</topic><topic>Radiation Tolerance</topic><topic>Reactive oxygen species</topic><topic>Signal Transduction - radiation effects</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumors</topic><topic>Ubiquitination</topic><topic>Up-Regulation</topic><topic>γ-IRRADIATION</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hassan, Mohamed</creatorcontrib><creatorcontrib>El Khattouti, Abdelouahid</creatorcontrib><creatorcontrib>Ejaeidi, Ahmed</creatorcontrib><creatorcontrib>Ma, Tangeng</creatorcontrib><creatorcontrib>Day, William A.</creatorcontrib><creatorcontrib>Espinoza, Ingrid</creatorcontrib><creatorcontrib>Vijayakumar, Srinivasan</creatorcontrib><creatorcontrib>Gomez, Christian R.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hassan, Mohamed</au><au>El Khattouti, Abdelouahid</au><au>Ejaeidi, Ahmed</au><au>Ma, Tangeng</au><au>Day, William A.</au><au>Espinoza, Ingrid</au><au>Vijayakumar, Srinivasan</au><au>Gomez, Christian R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Elevated Expression of Hepatoma Up-Regulated Protein Inhibits γ-Irradiation-Induced Apoptosis of Prostate Cancer Cells</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J. Cell. Biochem.</addtitle><date>2016-06</date><risdate>2016</risdate><volume>117</volume><issue>6</issue><spage>1308</spage><epage>1318</epage><pages>1308-1318</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>ABSTRACT
Despite progression in diagnosis and treatment, prostate cancer (PCa) still represents the main cause of cancer‐related mortality and morbidity in men. Although radiation therapy offers clinical benefit over other therapeutic modalities, the success of this therapeutic modality is commonly hampered by the resistance of advanced tumors. So far, the mechanisms governing tumor resistance to radiotherapy are not discussed in detail. Here, we demonstrate for the first time that the resistance of PCa to radiation therapy is attributed to elevated expression of Hepatoma Up‐Regulated Protein (HURP). In PCa cells, the induction of HURP expression suppresses γ‐irradiation‐induced apoptosis. γ‐irradiation‐induced apoptosis of PCa cells is associated with expression of E2F1, p53, p21 proteins together with the phosphorylation of apoptosis signal‐regulating kinase1 (ASK1), c‐jun‐N‐terminal kinase (JNK) and Ataxia‐telangiectasia mutated (ATM) and histone family member X (H2AX). Whereas, the induction of HURP expression is able to suppress γ‐irradiation‐induced effects on E2F1, p53, p21, ATM, ASK1, JNK and ATM, and H2AX. Also, inhibition of γ‐irradiation‐induced‐ cytochrome c release, cleavage of caspase‐9, caspase‐3, PARP, and reactive oxygen species (ROS) were noted in PCa cells induced for HURP expression. The observed radio‐resistance of PCa is thought to be the consequence of HURP‐mediated destabilization of p53 and ATM proteins that are essential for the modulation of γ‐irradiation‐induced apoptosis. Thus, based on our findings, PCa resistance to radiation therapy results from the deregulation of ASK1/ JNK; ATM/ H2AX; ATM/p53 and checkpoint kinase 2 (Chk2)/ E2F‐1 in response to the elevated expression of HURP. J. Cell. Biochem. 117: 1308–1318, 2016. © 2015 Wiley Periodicals, Inc.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>26505164</pmid><doi>10.1002/jcb.25419</doi><tpages>11</tpages></addata></record> |
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| subjects | APOPTOSIS ASK1 Ataxia Ataxia telangiectasia Ataxia telangiectasia mutated protein Ataxia Telangiectasia Mutated Proteins - metabolism Cancer therapies Caspase Cell Line, Tumor CHK2 protein Cyclin-dependent kinase inhibitor p21 Cytochrome c Cytochromes Deregulation Destabilization E2F1 protein Gamma Rays Gene Expression Regulation, Neoplastic Hepatoma Histone H2A Humans HURP Irradiation JNK JNK protein Kinases Liver cancer Male MAP kinase Morbidity Neoplasm Proteins - metabolism p53 Protein PCa Phosphorylation Poly(ADP-ribose) polymerase Prostate cancer Prostatic Neoplasms - metabolism Prostatic Neoplasms - radiotherapy Proteins Radiation therapy Radiation Tolerance Reactive oxygen species Signal Transduction - radiation effects Tumor Suppressor Protein p53 - metabolism Tumors Ubiquitination Up-Regulation γ-IRRADIATION |
| title | Elevated Expression of Hepatoma Up-Regulated Protein Inhibits γ-Irradiation-Induced Apoptosis of Prostate Cancer Cells |
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