BPIFB1 (LPLUNC1) inhibits radioresistance in nasopharyngeal carcinoma by inhibiting VTN expression
Bactericidal/permeability-increasing-fold-containing family B member 1 (BPIFB1, previously named LPLUNC1) is highly expressed in the nasopharynx and significantly downregulated in nasopharyngeal carcinoma (NPC). Low expression is also associated with poor prognosis in patients with NPC. Radiotherapy...
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| Veröffentlicht in: | Cell death & disease 2018-03, Vol.9 (4), p.432-12, Article 432 |
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| creator | Wei, Fang Tang, Le He, Yi Wu, Yingfen Shi, Lei Xiong, Fang Gong, Zhaojian Guo, Can Li, Xiayu Liao, Qianjin Zhang, Wenling Ni, Qianxi Luo, Jia Li, Xiaoling Li, Yong Peng, Cong Chen, Xiang Li, Guiyuan Xiong, Wei Zeng, Zhaoyang |
| description | Bactericidal/permeability-increasing-fold-containing family B member 1 (BPIFB1, previously named LPLUNC1) is highly expressed in the nasopharynx and significantly downregulated in nasopharyngeal carcinoma (NPC). Low expression is also associated with poor prognosis in patients with NPC. Radiotherapy is a routine treatment for NPC; however, radioresistance is a major cause of treatment failure. Thus, we aimed to investigate the role of BPIFB1 in the radioresponse of NPC. Colony formation and cell survival results showed that BPIFB1 sensitized NPC cells to ionizing radiation. VTN, a previously identified BPIFB1-binding protein, was shown to induce cell proliferation and survival, G2/M phase arrest, DNA repair, activation of the ATM-Chk2 and ATR-Chk1 pathways, and anti-apoptotic effects after exposure to radiation, facilitating NPC cell radioresistance. However, BPIFB1 inhibited this VTN-mediated radioresistance, ultimately improving NPC radiosensitivity. In conclusion, this study is the first to demonstrate the functions of BPIFB1 and VTN in the NPC radioresponse. Our findings indicated that promoting BPIFB1 expression and targeting VTN might represent new therapeutic strategies for NPC. |
| doi_str_mv | 10.1038/s41419-018-0409-0 |
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Low expression is also associated with poor prognosis in patients with NPC. Radiotherapy is a routine treatment for NPC; however, radioresistance is a major cause of treatment failure. Thus, we aimed to investigate the role of BPIFB1 in the radioresponse of NPC. Colony formation and cell survival results showed that BPIFB1 sensitized NPC cells to ionizing radiation. VTN, a previously identified BPIFB1-binding protein, was shown to induce cell proliferation and survival, G2/M phase arrest, DNA repair, activation of the ATM-Chk2 and ATR-Chk1 pathways, and anti-apoptotic effects after exposure to radiation, facilitating NPC cell radioresistance. However, BPIFB1 inhibited this VTN-mediated radioresistance, ultimately improving NPC radiosensitivity. In conclusion, this study is the first to demonstrate the functions of BPIFB1 and VTN in the NPC radioresponse. Our findings indicated that promoting BPIFB1 expression and targeting VTN might represent new therapeutic strategies for NPC.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-018-0409-0</identifier><identifier>PMID: 29568064</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/109 ; 13/2 ; 13/31 ; 13/95 ; 14 ; 14/1 ; 38 ; 38/1 ; 64 ; 82 ; Antibodies ; Apoptosis ; Apoptosis - radiation effects ; Ataxia Telangiectasia Mutated Proteins - metabolism ; Autoantigens - genetics ; Autoantigens - metabolism ; Biochemistry ; Biomedical and Life Sciences ; Cell Biology ; Cell Culture ; Cell Cycle Checkpoints - radiation effects ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - radiation effects ; Cell survival ; Checkpoint Kinase 1 - metabolism ; Checkpoint Kinase 2 - metabolism ; CHK1 protein ; DNA Repair ; Down-Regulation ; Fatty Acid-Binding Proteins - genetics ; Fatty Acid-Binding Proteins - metabolism ; Gene expression ; Humans ; Immunology ; Ionizing radiation ; Life Sciences ; Medical prognosis ; Nasopharyngeal carcinoma ; Nasopharyngeal Neoplasms - metabolism ; Nasopharyngeal Neoplasms - pathology ; Nasopharynx ; Permeability ; Radiation therapy ; Radiation Tolerance ; Radiation, Ionizing ; Radioresistance ; Radiosensitivity ; Signal Transduction - radiation effects ; Throat cancer ; Vitronectin - antagonists & inhibitors ; Vitronectin - genetics ; Vitronectin - metabolism</subject><ispartof>Cell death & disease, 2018-03, Vol.9 (4), p.432-12, Article 432</ispartof><rights>The Author(s) 2018</rights><rights>2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-965ba12923e2281c59eb41991e5a4fc1aa6791623c4ae773b818fb7ec35369dc3</citedby><cites>FETCH-LOGICAL-c470t-965ba12923e2281c59eb41991e5a4fc1aa6791623c4ae773b818fb7ec35369dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5864881/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5864881/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29568064$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wei, Fang</creatorcontrib><creatorcontrib>Tang, Le</creatorcontrib><creatorcontrib>He, Yi</creatorcontrib><creatorcontrib>Wu, Yingfen</creatorcontrib><creatorcontrib>Shi, Lei</creatorcontrib><creatorcontrib>Xiong, Fang</creatorcontrib><creatorcontrib>Gong, Zhaojian</creatorcontrib><creatorcontrib>Guo, Can</creatorcontrib><creatorcontrib>Li, Xiayu</creatorcontrib><creatorcontrib>Liao, Qianjin</creatorcontrib><creatorcontrib>Zhang, Wenling</creatorcontrib><creatorcontrib>Ni, Qianxi</creatorcontrib><creatorcontrib>Luo, Jia</creatorcontrib><creatorcontrib>Li, Xiaoling</creatorcontrib><creatorcontrib>Li, Yong</creatorcontrib><creatorcontrib>Peng, Cong</creatorcontrib><creatorcontrib>Chen, Xiang</creatorcontrib><creatorcontrib>Li, Guiyuan</creatorcontrib><creatorcontrib>Xiong, Wei</creatorcontrib><creatorcontrib>Zeng, Zhaoyang</creatorcontrib><title>BPIFB1 (LPLUNC1) inhibits radioresistance in nasopharyngeal carcinoma by inhibiting VTN expression</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Bactericidal/permeability-increasing-fold-containing family B member 1 (BPIFB1, previously named LPLUNC1) is highly expressed in the nasopharynx and significantly downregulated in nasopharyngeal carcinoma (NPC). Low expression is also associated with poor prognosis in patients with NPC. Radiotherapy is a routine treatment for NPC; however, radioresistance is a major cause of treatment failure. Thus, we aimed to investigate the role of BPIFB1 in the radioresponse of NPC. Colony formation and cell survival results showed that BPIFB1 sensitized NPC cells to ionizing radiation. VTN, a previously identified BPIFB1-binding protein, was shown to induce cell proliferation and survival, G2/M phase arrest, DNA repair, activation of the ATM-Chk2 and ATR-Chk1 pathways, and anti-apoptotic effects after exposure to radiation, facilitating NPC cell radioresistance. However, BPIFB1 inhibited this VTN-mediated radioresistance, ultimately improving NPC radiosensitivity. In conclusion, this study is the first to demonstrate the functions of BPIFB1 and VTN in the NPC radioresponse. Our findings indicated that promoting BPIFB1 expression and targeting VTN might represent new therapeutic strategies for NPC.</description><subject>13</subject><subject>13/109</subject><subject>13/2</subject><subject>13/31</subject><subject>13/95</subject><subject>14</subject><subject>14/1</subject><subject>38</subject><subject>38/1</subject><subject>64</subject><subject>82</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Apoptosis - radiation effects</subject><subject>Ataxia Telangiectasia Mutated Proteins - metabolism</subject><subject>Autoantigens - genetics</subject><subject>Autoantigens - metabolism</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell Cycle Checkpoints - radiation effects</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - radiation effects</subject><subject>Cell survival</subject><subject>Checkpoint Kinase 1 - 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metabolism</topic><topic>Nasopharyngeal Neoplasms - pathology</topic><topic>Nasopharynx</topic><topic>Permeability</topic><topic>Radiation therapy</topic><topic>Radiation Tolerance</topic><topic>Radiation, Ionizing</topic><topic>Radioresistance</topic><topic>Radiosensitivity</topic><topic>Signal Transduction - radiation effects</topic><topic>Throat cancer</topic><topic>Vitronectin - antagonists & inhibitors</topic><topic>Vitronectin - genetics</topic><topic>Vitronectin - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wei, Fang</creatorcontrib><creatorcontrib>Tang, Le</creatorcontrib><creatorcontrib>He, Yi</creatorcontrib><creatorcontrib>Wu, Yingfen</creatorcontrib><creatorcontrib>Shi, Lei</creatorcontrib><creatorcontrib>Xiong, Fang</creatorcontrib><creatorcontrib>Gong, Zhaojian</creatorcontrib><creatorcontrib>Guo, Can</creatorcontrib><creatorcontrib>Li, Xiayu</creatorcontrib><creatorcontrib>Liao, Qianjin</creatorcontrib><creatorcontrib>Zhang, Wenling</creatorcontrib><creatorcontrib>Ni, Qianxi</creatorcontrib><creatorcontrib>Luo, Jia</creatorcontrib><creatorcontrib>Li, Xiaoling</creatorcontrib><creatorcontrib>Li, Yong</creatorcontrib><creatorcontrib>Peng, Cong</creatorcontrib><creatorcontrib>Chen, Xiang</creatorcontrib><creatorcontrib>Li, Guiyuan</creatorcontrib><creatorcontrib>Xiong, Wei</creatorcontrib><creatorcontrib>Zeng, Zhaoyang</creatorcontrib><collection>Springer Nature OA Free Journals</collection><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content 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>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wei, Fang</au><au>Tang, Le</au><au>He, Yi</au><au>Wu, Yingfen</au><au>Shi, Lei</au><au>Xiong, Fang</au><au>Gong, Zhaojian</au><au>Guo, Can</au><au>Li, Xiayu</au><au>Liao, Qianjin</au><au>Zhang, Wenling</au><au>Ni, Qianxi</au><au>Luo, Jia</au><au>Li, Xiaoling</au><au>Li, Yong</au><au>Peng, Cong</au><au>Chen, Xiang</au><au>Li, Guiyuan</au><au>Xiong, Wei</au><au>Zeng, Zhaoyang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>BPIFB1 (LPLUNC1) inhibits radioresistance in nasopharyngeal carcinoma by inhibiting VTN expression</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2018-03-22</date><risdate>2018</risdate><volume>9</volume><issue>4</issue><spage>432</spage><epage>12</epage><pages>432-12</pages><artnum>432</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Bactericidal/permeability-increasing-fold-containing family B member 1 (BPIFB1, previously named LPLUNC1) is highly expressed in the nasopharynx and significantly downregulated in nasopharyngeal carcinoma (NPC). Low expression is also associated with poor prognosis in patients with NPC. Radiotherapy is a routine treatment for NPC; however, radioresistance is a major cause of treatment failure. Thus, we aimed to investigate the role of BPIFB1 in the radioresponse of NPC. Colony formation and cell survival results showed that BPIFB1 sensitized NPC cells to ionizing radiation. VTN, a previously identified BPIFB1-binding protein, was shown to induce cell proliferation and survival, G2/M phase arrest, DNA repair, activation of the ATM-Chk2 and ATR-Chk1 pathways, and anti-apoptotic effects after exposure to radiation, facilitating NPC cell radioresistance. However, BPIFB1 inhibited this VTN-mediated radioresistance, ultimately improving NPC radiosensitivity. In conclusion, this study is the first to demonstrate the functions of BPIFB1 and VTN in the NPC radioresponse. Our findings indicated that promoting BPIFB1 expression and targeting VTN might represent new therapeutic strategies for NPC.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29568064</pmid><doi>10.1038/s41419-018-0409-0</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13 13/109 13/2 13/31 13/95 14 14/1 38 38/1 64 82 Antibodies Apoptosis Apoptosis - radiation effects Ataxia Telangiectasia Mutated Proteins - metabolism Autoantigens - genetics Autoantigens - metabolism Biochemistry Biomedical and Life Sciences Cell Biology Cell Culture Cell Cycle Checkpoints - radiation effects Cell Line, Tumor Cell proliferation Cell Proliferation - radiation effects Cell survival Checkpoint Kinase 1 - metabolism Checkpoint Kinase 2 - metabolism CHK1 protein DNA Repair Down-Regulation Fatty Acid-Binding Proteins - genetics Fatty Acid-Binding Proteins - metabolism Gene expression Humans Immunology Ionizing radiation Life Sciences Medical prognosis Nasopharyngeal carcinoma Nasopharyngeal Neoplasms - metabolism Nasopharyngeal Neoplasms - pathology Nasopharynx Permeability Radiation therapy Radiation Tolerance Radiation, Ionizing Radioresistance Radiosensitivity Signal Transduction - radiation effects Throat cancer Vitronectin - antagonists & inhibitors Vitronectin - genetics Vitronectin - metabolism |
| title | BPIFB1 (LPLUNC1) inhibits radioresistance in nasopharyngeal carcinoma by inhibiting VTN expression |
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