Autophagy-Mediated Degradation of IAPs and c-FLIPL Potentiates Apoptosis Induced by Combination of TRAIL and Chal-24
ABSTRACT Combination chemotherapy is an effective strategy for increasing anticancer efficacy, reducing side effects and alleviating drug resistance. Here we report that combination of the recently identified novel chalcone derivative, chalcone‐24 (Chal‐24), and TNF‐related apoptosis‐inducing ligand...
Gespeichert in:
| Veröffentlicht in: | Journal of cellular biochemistry 2016-05, Vol.117 (5), p.1136-1144 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1144 |
|---|---|
| container_issue | 5 |
| container_start_page | 1136 |
| container_title | Journal of cellular biochemistry |
| container_volume | 117 |
| creator | Xu, Jennings Xu, Xiuling Shi, Shaoqing Wang, Qiong Saxton, Bryanna He, Weiyang Gou, Xin Jang, Jun-Ho Nyunoya, Toru Wang, Xia Xing, Chengguo Zhang, Lin Lin, Yong |
| description | ABSTRACT
Combination chemotherapy is an effective strategy for increasing anticancer efficacy, reducing side effects and alleviating drug resistance. Here we report that combination of the recently identified novel chalcone derivative, chalcone‐24 (Chal‐24), and TNF‐related apoptosis‐inducing ligand (TRAIL) significantly increases cytotoxicity in lung cancer cells. Chal‐24 treatment significantly enhanced TRAIL‐induced activation of caspase‐8 and caspase‐3, and the cytotoxicity induced by combination of these agents was effectively suppressed by the pan‐caspase inhibitor z‐VAD‐fmk. Chal‐24 and TRAIL combination suppressed expression of cellular FLICE (FADD‐like IL‐1β‐converting enzyme)‐inhibitory protein large (c‐FLIPL) and cellular inhibitor of apoptosis proteins (c‐IAPs), and ectopic expression of c‐FLIPL and c‐IAPs inhibited the potentiated cytotoxicity. In addition, TRAIL and Chal‐24 cooperatively activated autophagy. Suppression of autophagy effectively attenuated cytotoxicity induced by Chal‐24 and TRAIL combination, which was associated with attenuation of c‐FLIPL and c‐IAPs degradation. Altogether, these results suggest that Chal‐24 potentiates the anticancer activity of TRAIL through autophagy‐mediated degradation of c‐FLIPL and c‐IAPs, and that combination of Chal‐24 and TRAIL could be an effective approach in improving chemotherapy efficacy. J. Cell. Biochem. 117: 1136–1144, 2016. © 2015 Wiley Periodicals, Inc. |
| doi_str_mv | 10.1002/jcb.25397 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4894717</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3969752551</sourcerecordid><originalsourceid>FETCH-LOGICAL-i4797-122f5bd44198b2a137b58e8ad114e7ced83979b20869dcfb76e8331f342e27963</originalsourceid><addsrcrecordid>eNpVUU1v00AQXSFQG0IP_AMLzm73y177gmQMLUYORG0Rx9V-OdmQeF3vmjb_nm1SReI0I817b-bNA-A9gpcIQny1UfISZ6Rkr8AMwZKlNKf0NZhBRmCKCcLn4K33GwhhWRJ8Bs5xnBc5LGYgVFNww1qs9unCaCuC0ckXsxqFFsG6PnFd0lRLn4heJyq9bptlmyxdMH14xvqkGtwQnLc-aXo9qciW-6R2O2n7k8D9bdW0B4V6LbYppu_Am05svbl4qXPw6_rrff0tbX_eNHXVppay6AJh3GVSU4rKQmKBCJNZYQqhEaKGxV1FtFxKDIu81KqTLDcFIagjFBvMypzMwaej7jDJndEqXj2KLR9GuxPjnjth-f-T3q75yv3ltCgpQywKfDgKOB8s98oGo9bK9b1RgSNCMxzfPgcfX7aM7mEyPvCNm8Y-GuOIsZgPyhiKqKsj6tFuzf50A4L8OUIeI-SHCPn3-vOhiYz0yLA-mKcTQ4x_eM4Iy_jvHzd8gVtI7tiCL8g_Pe6cRA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1770021571</pqid></control><display><type>article</type><title>Autophagy-Mediated Degradation of IAPs and c-FLIPL Potentiates Apoptosis Induced by Combination of TRAIL and Chal-24</title><source>Wiley Online Library Journals Frontfile Complete</source><creator>Xu, Jennings ; Xu, Xiuling ; Shi, Shaoqing ; Wang, Qiong ; Saxton, Bryanna ; He, Weiyang ; Gou, Xin ; Jang, Jun-Ho ; Nyunoya, Toru ; Wang, Xia ; Xing, Chengguo ; Zhang, Lin ; Lin, Yong</creator><creatorcontrib>Xu, Jennings ; Xu, Xiuling ; Shi, Shaoqing ; Wang, Qiong ; Saxton, Bryanna ; He, Weiyang ; Gou, Xin ; Jang, Jun-Ho ; Nyunoya, Toru ; Wang, Xia ; Xing, Chengguo ; Zhang, Lin ; Lin, Yong ; Lovelace Respiratory Research Inst., Albuquerque, NM (United States)</creatorcontrib><description>ABSTRACT
Combination chemotherapy is an effective strategy for increasing anticancer efficacy, reducing side effects and alleviating drug resistance. Here we report that combination of the recently identified novel chalcone derivative, chalcone‐24 (Chal‐24), and TNF‐related apoptosis‐inducing ligand (TRAIL) significantly increases cytotoxicity in lung cancer cells. Chal‐24 treatment significantly enhanced TRAIL‐induced activation of caspase‐8 and caspase‐3, and the cytotoxicity induced by combination of these agents was effectively suppressed by the pan‐caspase inhibitor z‐VAD‐fmk. Chal‐24 and TRAIL combination suppressed expression of cellular FLICE (FADD‐like IL‐1β‐converting enzyme)‐inhibitory protein large (c‐FLIPL) and cellular inhibitor of apoptosis proteins (c‐IAPs), and ectopic expression of c‐FLIPL and c‐IAPs inhibited the potentiated cytotoxicity. In addition, TRAIL and Chal‐24 cooperatively activated autophagy. Suppression of autophagy effectively attenuated cytotoxicity induced by Chal‐24 and TRAIL combination, which was associated with attenuation of c‐FLIPL and c‐IAPs degradation. Altogether, these results suggest that Chal‐24 potentiates the anticancer activity of TRAIL through autophagy‐mediated degradation of c‐FLIPL and c‐IAPs, and that combination of Chal‐24 and TRAIL could be an effective approach in improving chemotherapy efficacy. J. Cell. Biochem. 117: 1136–1144, 2016. © 2015 Wiley Periodicals, Inc.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.25397</identifier><identifier>PMID: 26448608</identifier><language>eng</language><publisher>Hoboken: Blackwell Publishing Ltd</publisher><subject>APOPTOSIS ; AUTOPHAGY ; BASIC BIOLOGICAL SCIENCES ; c-FLIP ; c-IAP ; CHAL-24 ; TRAIL</subject><ispartof>Journal of cellular biochemistry, 2016-05, Vol.117 (5), p.1136-1144</ispartof><rights>2015 Wiley Periodicals, Inc.</rights><rights>2016 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></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.25397$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.25397$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.osti.gov/servlets/purl/1345225$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Jennings</creatorcontrib><creatorcontrib>Xu, Xiuling</creatorcontrib><creatorcontrib>Shi, Shaoqing</creatorcontrib><creatorcontrib>Wang, Qiong</creatorcontrib><creatorcontrib>Saxton, Bryanna</creatorcontrib><creatorcontrib>He, Weiyang</creatorcontrib><creatorcontrib>Gou, Xin</creatorcontrib><creatorcontrib>Jang, Jun-Ho</creatorcontrib><creatorcontrib>Nyunoya, Toru</creatorcontrib><creatorcontrib>Wang, Xia</creatorcontrib><creatorcontrib>Xing, Chengguo</creatorcontrib><creatorcontrib>Zhang, Lin</creatorcontrib><creatorcontrib>Lin, Yong</creatorcontrib><creatorcontrib>Lovelace Respiratory Research Inst., Albuquerque, NM (United States)</creatorcontrib><title>Autophagy-Mediated Degradation of IAPs and c-FLIPL Potentiates Apoptosis Induced by Combination of TRAIL and Chal-24</title><title>Journal of cellular biochemistry</title><addtitle>J. Cell. Biochem</addtitle><description>ABSTRACT
Combination chemotherapy is an effective strategy for increasing anticancer efficacy, reducing side effects and alleviating drug resistance. Here we report that combination of the recently identified novel chalcone derivative, chalcone‐24 (Chal‐24), and TNF‐related apoptosis‐inducing ligand (TRAIL) significantly increases cytotoxicity in lung cancer cells. Chal‐24 treatment significantly enhanced TRAIL‐induced activation of caspase‐8 and caspase‐3, and the cytotoxicity induced by combination of these agents was effectively suppressed by the pan‐caspase inhibitor z‐VAD‐fmk. Chal‐24 and TRAIL combination suppressed expression of cellular FLICE (FADD‐like IL‐1β‐converting enzyme)‐inhibitory protein large (c‐FLIPL) and cellular inhibitor of apoptosis proteins (c‐IAPs), and ectopic expression of c‐FLIPL and c‐IAPs inhibited the potentiated cytotoxicity. In addition, TRAIL and Chal‐24 cooperatively activated autophagy. Suppression of autophagy effectively attenuated cytotoxicity induced by Chal‐24 and TRAIL combination, which was associated with attenuation of c‐FLIPL and c‐IAPs degradation. Altogether, these results suggest that Chal‐24 potentiates the anticancer activity of TRAIL through autophagy‐mediated degradation of c‐FLIPL and c‐IAPs, and that combination of Chal‐24 and TRAIL could be an effective approach in improving chemotherapy efficacy. J. Cell. Biochem. 117: 1136–1144, 2016. © 2015 Wiley Periodicals, Inc.</description><subject>APOPTOSIS</subject><subject>AUTOPHAGY</subject><subject>BASIC BIOLOGICAL SCIENCES</subject><subject>c-FLIP</subject><subject>c-IAP</subject><subject>CHAL-24</subject><subject>TRAIL</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNpVUU1v00AQXSFQG0IP_AMLzm73y177gmQMLUYORG0Rx9V-OdmQeF3vmjb_nm1SReI0I817b-bNA-A9gpcIQny1UfISZ6Rkr8AMwZKlNKf0NZhBRmCKCcLn4K33GwhhWRJ8Bs5xnBc5LGYgVFNww1qs9unCaCuC0ckXsxqFFsG6PnFd0lRLn4heJyq9bptlmyxdMH14xvqkGtwQnLc-aXo9qciW-6R2O2n7k8D9bdW0B4V6LbYppu_Am05svbl4qXPw6_rrff0tbX_eNHXVppay6AJh3GVSU4rKQmKBCJNZYQqhEaKGxV1FtFxKDIu81KqTLDcFIagjFBvMypzMwaej7jDJndEqXj2KLR9GuxPjnjth-f-T3q75yv3ltCgpQywKfDgKOB8s98oGo9bK9b1RgSNCMxzfPgcfX7aM7mEyPvCNm8Y-GuOIsZgPyhiKqKsj6tFuzf50A4L8OUIeI-SHCPn3-vOhiYz0yLA-mKcTQ4x_eM4Iy_jvHzd8gVtI7tiCL8g_Pe6cRA</recordid><startdate>201605</startdate><enddate>201605</enddate><creator>Xu, Jennings</creator><creator>Xu, Xiuling</creator><creator>Shi, Shaoqing</creator><creator>Wang, Qiong</creator><creator>Saxton, Bryanna</creator><creator>He, Weiyang</creator><creator>Gou, Xin</creator><creator>Jang, Jun-Ho</creator><creator>Nyunoya, Toru</creator><creator>Wang, Xia</creator><creator>Xing, Chengguo</creator><creator>Zhang, Lin</creator><creator>Lin, Yong</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><general>Wiley</general><scope>BSCLL</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>OIOZB</scope><scope>OTOTI</scope><scope>5PM</scope></search><sort><creationdate>201605</creationdate><title>Autophagy-Mediated Degradation of IAPs and c-FLIPL Potentiates Apoptosis Induced by Combination of TRAIL and Chal-24</title><author>Xu, Jennings ; Xu, Xiuling ; Shi, Shaoqing ; Wang, Qiong ; Saxton, Bryanna ; He, Weiyang ; Gou, Xin ; Jang, Jun-Ho ; Nyunoya, Toru ; Wang, Xia ; Xing, Chengguo ; Zhang, Lin ; Lin, Yong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i4797-122f5bd44198b2a137b58e8ad114e7ced83979b20869dcfb76e8331f342e27963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>APOPTOSIS</topic><topic>AUTOPHAGY</topic><topic>BASIC BIOLOGICAL SCIENCES</topic><topic>c-FLIP</topic><topic>c-IAP</topic><topic>CHAL-24</topic><topic>TRAIL</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Jennings</creatorcontrib><creatorcontrib>Xu, Xiuling</creatorcontrib><creatorcontrib>Shi, Shaoqing</creatorcontrib><creatorcontrib>Wang, Qiong</creatorcontrib><creatorcontrib>Saxton, Bryanna</creatorcontrib><creatorcontrib>He, Weiyang</creatorcontrib><creatorcontrib>Gou, Xin</creatorcontrib><creatorcontrib>Jang, Jun-Ho</creatorcontrib><creatorcontrib>Nyunoya, Toru</creatorcontrib><creatorcontrib>Wang, Xia</creatorcontrib><creatorcontrib>Xing, Chengguo</creatorcontrib><creatorcontrib>Zhang, Lin</creatorcontrib><creatorcontrib>Lin, Yong</creatorcontrib><creatorcontrib>Lovelace Respiratory Research Inst., Albuquerque, NM (United States)</creatorcontrib><collection>Istex</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>OSTI.GOV - Hybrid</collection><collection>OSTI.GOV</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Jennings</au><au>Xu, Xiuling</au><au>Shi, Shaoqing</au><au>Wang, Qiong</au><au>Saxton, Bryanna</au><au>He, Weiyang</au><au>Gou, Xin</au><au>Jang, Jun-Ho</au><au>Nyunoya, Toru</au><au>Wang, Xia</au><au>Xing, Chengguo</au><au>Zhang, Lin</au><au>Lin, Yong</au><aucorp>Lovelace Respiratory Research Inst., Albuquerque, NM (United States)</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autophagy-Mediated Degradation of IAPs and c-FLIPL Potentiates Apoptosis Induced by Combination of TRAIL and Chal-24</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J. Cell. Biochem</addtitle><date>2016-05</date><risdate>2016</risdate><volume>117</volume><issue>5</issue><spage>1136</spage><epage>1144</epage><pages>1136-1144</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>ABSTRACT
Combination chemotherapy is an effective strategy for increasing anticancer efficacy, reducing side effects and alleviating drug resistance. Here we report that combination of the recently identified novel chalcone derivative, chalcone‐24 (Chal‐24), and TNF‐related apoptosis‐inducing ligand (TRAIL) significantly increases cytotoxicity in lung cancer cells. Chal‐24 treatment significantly enhanced TRAIL‐induced activation of caspase‐8 and caspase‐3, and the cytotoxicity induced by combination of these agents was effectively suppressed by the pan‐caspase inhibitor z‐VAD‐fmk. Chal‐24 and TRAIL combination suppressed expression of cellular FLICE (FADD‐like IL‐1β‐converting enzyme)‐inhibitory protein large (c‐FLIPL) and cellular inhibitor of apoptosis proteins (c‐IAPs), and ectopic expression of c‐FLIPL and c‐IAPs inhibited the potentiated cytotoxicity. In addition, TRAIL and Chal‐24 cooperatively activated autophagy. Suppression of autophagy effectively attenuated cytotoxicity induced by Chal‐24 and TRAIL combination, which was associated with attenuation of c‐FLIPL and c‐IAPs degradation. Altogether, these results suggest that Chal‐24 potentiates the anticancer activity of TRAIL through autophagy‐mediated degradation of c‐FLIPL and c‐IAPs, and that combination of Chal‐24 and TRAIL could be an effective approach in improving chemotherapy efficacy. J. Cell. Biochem. 117: 1136–1144, 2016. © 2015 Wiley Periodicals, Inc.</abstract><cop>Hoboken</cop><pub>Blackwell Publishing Ltd</pub><pmid>26448608</pmid><doi>10.1002/jcb.25397</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0730-2312 |
| ispartof | Journal of cellular biochemistry, 2016-05, Vol.117 (5), p.1136-1144 |
| issn | 0730-2312 1097-4644 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4894717 |
| source | Wiley Online Library Journals Frontfile Complete |
| subjects | APOPTOSIS AUTOPHAGY BASIC BIOLOGICAL SCIENCES c-FLIP c-IAP CHAL-24 TRAIL |
| title | Autophagy-Mediated Degradation of IAPs and c-FLIPL Potentiates Apoptosis Induced by Combination of TRAIL and Chal-24 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-23T13%3A21%3A44IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Autophagy-Mediated%20Degradation%20of%20IAPs%20and%20c-FLIPL%20Potentiates%20Apoptosis%20Induced%20by%20Combination%20of%20TRAIL%20and%20Chal-24&rft.jtitle=Journal%20of%20cellular%20biochemistry&rft.au=Xu,%20Jennings&rft.aucorp=Lovelace%20Respiratory%20Research%20Inst.,%20Albuquerque,%20NM%20(United%20States)&rft.date=2016-05&rft.volume=117&rft.issue=5&rft.spage=1136&rft.epage=1144&rft.pages=1136-1144&rft.issn=0730-2312&rft.eissn=1097-4644&rft_id=info:doi/10.1002/jcb.25397&rft_dat=%3Cproquest_pubme%3E3969752551%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1770021571&rft_id=info:pmid/26448608&rfr_iscdi=true |