Overexpressed nuclear BAG-1 in human hepatocellular carcinoma is associated with poor prognosis and resistance to doxorubicin
Bcl‐2‐associated athanogene‐1 (BAG‐1) is a multifunctional anti‐apoptotic protein which regulates an array of cellular processes, including apoptosis, signaling, proliferation, transcription, and cell motility and has been reported to be over‐expressed in a number of human malignancies. To investiga...
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| Veröffentlicht in: | Journal of cellular biochemistry 2013-09, Vol.114 (9), p.2120-2130 |
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| container_title | Journal of cellular biochemistry |
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| creator | Ni, Wenkai Chen, Buyou Zhou, Guoxiong Lu, Cuihua Xiao, Mingbing Guan, Chengqi Zhang, Yixing He, Song Shen, Aiguo Ni, Runzhou |
| description | Bcl‐2‐associated athanogene‐1 (BAG‐1) is a multifunctional anti‐apoptotic protein which regulates an array of cellular processes, including apoptosis, signaling, proliferation, transcription, and cell motility and has been reported to be over‐expressed in a number of human malignancies. To investigate the possible involvement of BAG‐1 in tumorigenesis of hepatocellular carcinoma (HCC), we performed Western blot analysis in eight paired samples of HCC and adjacent peritumoral tissues and immunohistochemistry in 65 paraffin sections of HCC, which both showed an enhanced expression of nuclear BAG‐1 isoform in HCC tissues. Statistical analysis confirmed that overexpression of nuclear BAG‐1 in HCC tissues was significantly associated with histological grading (P |
| doi_str_mv | 10.1002/jcb.24560 |
| format | Article |
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To investigate the possible involvement of BAG‐1 in tumorigenesis of hepatocellular carcinoma (HCC), we performed Western blot analysis in eight paired samples of HCC and adjacent peritumoral tissues and immunohistochemistry in 65 paraffin sections of HCC, which both showed an enhanced expression of nuclear BAG‐1 isoform in HCC tissues. Statistical analysis confirmed that overexpression of nuclear BAG‐1 in HCC tissues was significantly associated with histological grading (P < 0.001), poor prognosis (P = 0.004), and was found to be an independent prognostic indicator for HCC (P = 0.023). We also noted that BAG‐1 was overexpressed in four HCC cell lines compared with a normal hepatocyte cell line, and BAG‐1 overexpression increased resistance of HCC cells to doxorubicin, a common chemotherapeutic agent for HCC. Furthermore, we observed that knock down of BAG‐1 with siRNA in HepG2 cells increased the chemosensitivity of cells, a process mediated through inhibition of doxorubicin‐triggered NF‐κB activation; and knock down of BAG‐1 suppressed proliferation and cell cycle transition of HepG2 cells. In consequence, our results for the first time indicated that BAG‐1 was dysregulated in HCC and suppression of BAG‐1 expression which resulted in inhibiting of NF‐κB signaling might be developed into a new strategy in HCC therapy. J. Cell. Biochem. 114: 2120–2130, 2013. © 2013 Wiley Periodicals, Inc.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.24560</identifier><identifier>PMID: 23553841</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Adult ; Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Apoptosis - drug effects ; BCL-2-ASSOCIATED ATHANOGENE-1 (BAG-1) ; Carcinoma, Hepatocellular - drug therapy ; Carcinoma, Hepatocellular - metabolism ; Cell Cycle - drug effects ; Cell Cycle - genetics ; CHEMORESISTANCE ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Doxorubicin - pharmacology ; Doxorubicin - therapeutic use ; Drug Resistance, Neoplasm - genetics ; Female ; Hep G2 Cells ; HEPATOCELLULAR CARCINOMA (HCC) ; Humans ; Immunohistochemistry ; In Vitro Techniques ; Liver Neoplasms - drug therapy ; Liver Neoplasms - metabolism ; Male ; Middle Aged ; NUCLEAR FACTOR-κB (NF-κB) ; PROGNOSIS ; RNA, Small Interfering - genetics ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Young Adult</subject><ispartof>Journal of cellular biochemistry, 2013-09, Vol.114 (9), p.2120-2130</ispartof><rights>Copyright © 2013 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3910-d778db2170fac05c46856a21b701d2ba49d4c55e3c76d16c346a9fb1bb0d2133</citedby><cites>FETCH-LOGICAL-c3910-d778db2170fac05c46856a21b701d2ba49d4c55e3c76d16c346a9fb1bb0d2133</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.24560$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.24560$$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/23553841$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ni, Wenkai</creatorcontrib><creatorcontrib>Chen, Buyou</creatorcontrib><creatorcontrib>Zhou, Guoxiong</creatorcontrib><creatorcontrib>Lu, Cuihua</creatorcontrib><creatorcontrib>Xiao, Mingbing</creatorcontrib><creatorcontrib>Guan, Chengqi</creatorcontrib><creatorcontrib>Zhang, Yixing</creatorcontrib><creatorcontrib>He, Song</creatorcontrib><creatorcontrib>Shen, Aiguo</creatorcontrib><creatorcontrib>Ni, Runzhou</creatorcontrib><title>Overexpressed nuclear BAG-1 in human hepatocellular carcinoma is associated with poor prognosis and resistance to doxorubicin</title><title>Journal of cellular biochemistry</title><addtitle>J. Cell. Biochem</addtitle><description>Bcl‐2‐associated athanogene‐1 (BAG‐1) is a multifunctional anti‐apoptotic protein which regulates an array of cellular processes, including apoptosis, signaling, proliferation, transcription, and cell motility and has been reported to be over‐expressed in a number of human malignancies. To investigate the possible involvement of BAG‐1 in tumorigenesis of hepatocellular carcinoma (HCC), we performed Western blot analysis in eight paired samples of HCC and adjacent peritumoral tissues and immunohistochemistry in 65 paraffin sections of HCC, which both showed an enhanced expression of nuclear BAG‐1 isoform in HCC tissues. Statistical analysis confirmed that overexpression of nuclear BAG‐1 in HCC tissues was significantly associated with histological grading (P < 0.001), poor prognosis (P = 0.004), and was found to be an independent prognostic indicator for HCC (P = 0.023). We also noted that BAG‐1 was overexpressed in four HCC cell lines compared with a normal hepatocyte cell line, and BAG‐1 overexpression increased resistance of HCC cells to doxorubicin, a common chemotherapeutic agent for HCC. Furthermore, we observed that knock down of BAG‐1 with siRNA in HepG2 cells increased the chemosensitivity of cells, a process mediated through inhibition of doxorubicin‐triggered NF‐κB activation; and knock down of BAG‐1 suppressed proliferation and cell cycle transition of HepG2 cells. In consequence, our results for the first time indicated that BAG‐1 was dysregulated in HCC and suppression of BAG‐1 expression which resulted in inhibiting of NF‐κB signaling might be developed into a new strategy in HCC therapy. J. Cell. Biochem. 114: 2120–2130, 2013. © 2013 Wiley Periodicals, Inc.</description><subject>Adult</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Apoptosis - drug effects</subject><subject>BCL-2-ASSOCIATED ATHANOGENE-1 (BAG-1)</subject><subject>Carcinoma, Hepatocellular - drug therapy</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Cycle - genetics</subject><subject>CHEMORESISTANCE</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Doxorubicin - pharmacology</subject><subject>Doxorubicin - therapeutic use</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Female</subject><subject>Hep G2 Cells</subject><subject>HEPATOCELLULAR CARCINOMA (HCC)</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>In Vitro Techniques</subject><subject>Liver Neoplasms - drug therapy</subject><subject>Liver Neoplasms - metabolism</subject><subject>Male</subject><subject>Middle Aged</subject><subject>NUCLEAR FACTOR-κB (NF-κB)</subject><subject>PROGNOSIS</subject><subject>RNA, Small Interfering - genetics</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Young Adult</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU9v0zAYhy3ExMrgwBdAlrjAIdvrP7GT41pBx1RtEqrgaDm2y1ySOLMT1h347rh02wFpF_vwPr9Hr_1D6B2BUwJAz7amOaW8FPACzQjUsuCC85doBpJBQRmhx-h1SlsAqGtGX6FjysqSVZzM0J_r3y663RBdSs7ifjKt0xHPz5cFwb7HN1On8-kGPQbj2nZq89ToaHwfOo19wjqlYLwec_rOjzd4CCHiIYaffUj7cW9xlvs06t44PAZswy7EqfFZ8QYdbXSb3NuH-wStv3xeLy6K1fXy6-J8VRhWEyislJVtKJGw0QZKw0VVCk1JI4FY2mheW27K0jEjhSXCMC50vWlI04ClhLET9PGgzWvdTi6NqvNp_xrduzAlRTghglYlg4x--A_dhin2eblMAVTZRmWmPh0oE0NK0W3UEH2n470ioPaVqFyJ-ldJZt8_GKemc_aJfOwgA2cH4M637v55k7pczB-VxSGRf9XtnhI6_lJCMlmqH1dLdUGX8-_r1TdF2F9EXaU7</recordid><startdate>201309</startdate><enddate>201309</enddate><creator>Ni, Wenkai</creator><creator>Chen, Buyou</creator><creator>Zhou, Guoxiong</creator><creator>Lu, Cuihua</creator><creator>Xiao, Mingbing</creator><creator>Guan, Chengqi</creator><creator>Zhang, Yixing</creator><creator>He, Song</creator><creator>Shen, Aiguo</creator><creator>Ni, Runzhou</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>201309</creationdate><title>Overexpressed nuclear BAG-1 in human hepatocellular carcinoma is associated with poor prognosis and resistance to doxorubicin</title><author>Ni, Wenkai ; 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Cell. Biochem</addtitle><date>2013-09</date><risdate>2013</risdate><volume>114</volume><issue>9</issue><spage>2120</spage><epage>2130</epage><pages>2120-2130</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>Bcl‐2‐associated athanogene‐1 (BAG‐1) is a multifunctional anti‐apoptotic protein which regulates an array of cellular processes, including apoptosis, signaling, proliferation, transcription, and cell motility and has been reported to be over‐expressed in a number of human malignancies. To investigate the possible involvement of BAG‐1 in tumorigenesis of hepatocellular carcinoma (HCC), we performed Western blot analysis in eight paired samples of HCC and adjacent peritumoral tissues and immunohistochemistry in 65 paraffin sections of HCC, which both showed an enhanced expression of nuclear BAG‐1 isoform in HCC tissues. Statistical analysis confirmed that overexpression of nuclear BAG‐1 in HCC tissues was significantly associated with histological grading (P < 0.001), poor prognosis (P = 0.004), and was found to be an independent prognostic indicator for HCC (P = 0.023). We also noted that BAG‐1 was overexpressed in four HCC cell lines compared with a normal hepatocyte cell line, and BAG‐1 overexpression increased resistance of HCC cells to doxorubicin, a common chemotherapeutic agent for HCC. Furthermore, we observed that knock down of BAG‐1 with siRNA in HepG2 cells increased the chemosensitivity of cells, a process mediated through inhibition of doxorubicin‐triggered NF‐κB activation; and knock down of BAG‐1 suppressed proliferation and cell cycle transition of HepG2 cells. In consequence, our results for the first time indicated that BAG‐1 was dysregulated in HCC and suppression of BAG‐1 expression which resulted in inhibiting of NF‐κB signaling might be developed into a new strategy in HCC therapy. J. Cell. Biochem. 114: 2120–2130, 2013. © 2013 Wiley Periodicals, Inc.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>23553841</pmid><doi>10.1002/jcb.24560</doi><tpages>11</tpages></addata></record> |
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| ispartof | Journal of cellular biochemistry, 2013-09, Vol.114 (9), p.2120-2130 |
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| subjects | Adult Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Apoptosis - drug effects BCL-2-ASSOCIATED ATHANOGENE-1 (BAG-1) Carcinoma, Hepatocellular - drug therapy Carcinoma, Hepatocellular - metabolism Cell Cycle - drug effects Cell Cycle - genetics CHEMORESISTANCE DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Doxorubicin - pharmacology Doxorubicin - therapeutic use Drug Resistance, Neoplasm - genetics Female Hep G2 Cells HEPATOCELLULAR CARCINOMA (HCC) Humans Immunohistochemistry In Vitro Techniques Liver Neoplasms - drug therapy Liver Neoplasms - metabolism Male Middle Aged NUCLEAR FACTOR-κB (NF-κB) PROGNOSIS RNA, Small Interfering - genetics Transcription Factors - genetics Transcription Factors - metabolism Young Adult |
| title | Overexpressed nuclear BAG-1 in human hepatocellular carcinoma is associated with poor prognosis and resistance to doxorubicin |
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