(-)-Guaiol regulates RAD51 stability via autophagy to induce cell apoptosis in non-small cell lung cancer
(-)-Guaiol, generally known as an antibacterial compound, has been found in many medicinal plants. Its roles in tumor suppression are still under investigation. In the study, we mainly focused on exploring its applications in dealing with non-small cell lung cancer (NSCLC) and the underlying mechani...
Gespeichert in:
| Veröffentlicht in: | Oncotarget 2016-09, Vol.7 (38), p.62585-62597 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 62597 |
|---|---|
| container_issue | 38 |
| container_start_page | 62585 |
| container_title | Oncotarget |
| container_volume | 7 |
| creator | Yang, Qingyuan Wu, Jianchun Luo, Yingbin Huang, Nan Zhen, Ni Zhou, Yun Sun, Fenyong Li, Zhi Pan, Qiuhui Li, Yan |
| description | (-)-Guaiol, generally known as an antibacterial compound, has been found in many medicinal plants. Its roles in tumor suppression are still under investigation. In the study, we mainly focused on exploring its applications in dealing with non-small cell lung cancer (NSCLC) and the underlying mechanisms. Here, we show that (-)-Guaiol significantly inhibits cell growth of NSCLC cells both in vitro and in vivo. Further high throughput analysis reveals that RAD51, a pivotal factor in homologous recombination repair, is a potential target for it. The following mechanism studies show that (-)-Guaiol is involved in cell autophagy to regulate the expression of RAD51, leading to double-strand breaks triggered cell apoptosis. Moreover, targeting RAD51, which is highly overexpressed in the lung adenocarcinoma tissues, can significantly increase the chemosensitivity of NSCLC cells to (-)-Guaiol both in vitro and in vivo. All in all, our studies provide an attractive insight in applying (-)-Guaiol into NSCLC treatments and further suggest that knockdown of oncogenic RAD51 will greatly enhance the chemosensitivity of patients with NSCLC. |
| doi_str_mv | 10.18632/oncotarget.11540 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5308748</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1854802576</sourcerecordid><originalsourceid>FETCH-LOGICAL-c356t-490ba4fb59854e6922e5eac8975cc71907d7e83f974e8a8919387fe588e0a2753</originalsourceid><addsrcrecordid>eNpVUU1LxDAQDaKoqD_Ai-Soh2rSNk1yEcRvEATRc5jNTmukm9QkFfbfW9fvuczw3sybGR4h-5wdc9VU5UnwNmSIHeZjzkXN1sg217UuSiGq9T_1FtlL6YVNIWqpSr1JtkopmkZIvU3cYXFUXI_gQk8jdmMPGRN9OLsQnKYMM9e7vKRvDiiMOQzP0C1pDtT5-WiRWux7CkMYckguTSj1wRdpARO84vrRd9SCtxh3yUYLfcK9r7xDnq4uH89virv769vzs7vCVqLJRa3ZDOp2JrQSNTa6LFEgWKWlsFZyzeRcoqpaLWtUoDTXlZItCqWQwfRXtUNOP3WHcbbAuUWfI_RmiG4BcWkCOPOf8e7ZdOHNiIopWatJ4PBLIIbXEVM2C5c-vgGPYUyGT4cpVgrZTK38s9XGkFLE9mcNZ2blkvl1yaxcmmYO_t73M_HtSfUOTzqRXQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1854802576</pqid></control><display><type>article</type><title>(-)-Guaiol regulates RAD51 stability via autophagy to induce cell apoptosis in non-small cell lung cancer</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Free E- Journals</source><source>PubMed Central Open Access</source><creator>Yang, Qingyuan ; Wu, Jianchun ; Luo, Yingbin ; Huang, Nan ; Zhen, Ni ; Zhou, Yun ; Sun, Fenyong ; Li, Zhi ; Pan, Qiuhui ; Li, Yan</creator><creatorcontrib>Yang, Qingyuan ; Wu, Jianchun ; Luo, Yingbin ; Huang, Nan ; Zhen, Ni ; Zhou, Yun ; Sun, Fenyong ; Li, Zhi ; Pan, Qiuhui ; Li, Yan</creatorcontrib><description>(-)-Guaiol, generally known as an antibacterial compound, has been found in many medicinal plants. Its roles in tumor suppression are still under investigation. In the study, we mainly focused on exploring its applications in dealing with non-small cell lung cancer (NSCLC) and the underlying mechanisms. Here, we show that (-)-Guaiol significantly inhibits cell growth of NSCLC cells both in vitro and in vivo. Further high throughput analysis reveals that RAD51, a pivotal factor in homologous recombination repair, is a potential target for it. The following mechanism studies show that (-)-Guaiol is involved in cell autophagy to regulate the expression of RAD51, leading to double-strand breaks triggered cell apoptosis. Moreover, targeting RAD51, which is highly overexpressed in the lung adenocarcinoma tissues, can significantly increase the chemosensitivity of NSCLC cells to (-)-Guaiol both in vitro and in vivo. All in all, our studies provide an attractive insight in applying (-)-Guaiol into NSCLC treatments and further suggest that knockdown of oncogenic RAD51 will greatly enhance the chemosensitivity of patients with NSCLC.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.11540</identifier><identifier>PMID: 27566579</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>Adenocarcinoma - drug therapy ; Adenocarcinoma - metabolism ; Adenocarcinoma of Lung ; Animals ; Antineoplastic Agents - chemistry ; Apoptosis ; Autophagy ; Carcinoma, Non-Small-Cell Lung - drug therapy ; Carcinoma, Non-Small-Cell Lung - metabolism ; Cell Line, Tumor ; DNA Breaks, Double-Stranded ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms - drug therapy ; Lung Neoplasms - metabolism ; Lysosomes - metabolism ; Male ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Oncogenes ; Rad51 Recombinase - metabolism ; Recombination, Genetic ; Research Paper ; Sesquiterpenes - pharmacology</subject><ispartof>Oncotarget, 2016-09, Vol.7 (38), p.62585-62597</ispartof><rights>Copyright: © 2016 Yang et al. 2016</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-490ba4fb59854e6922e5eac8975cc71907d7e83f974e8a8919387fe588e0a2753</citedby><cites>FETCH-LOGICAL-c356t-490ba4fb59854e6922e5eac8975cc71907d7e83f974e8a8919387fe588e0a2753</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/PMC5308748/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5308748/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27566579$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Qingyuan</creatorcontrib><creatorcontrib>Wu, Jianchun</creatorcontrib><creatorcontrib>Luo, Yingbin</creatorcontrib><creatorcontrib>Huang, Nan</creatorcontrib><creatorcontrib>Zhen, Ni</creatorcontrib><creatorcontrib>Zhou, Yun</creatorcontrib><creatorcontrib>Sun, Fenyong</creatorcontrib><creatorcontrib>Li, Zhi</creatorcontrib><creatorcontrib>Pan, Qiuhui</creatorcontrib><creatorcontrib>Li, Yan</creatorcontrib><title>(-)-Guaiol regulates RAD51 stability via autophagy to induce cell apoptosis in non-small cell lung cancer</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>(-)-Guaiol, generally known as an antibacterial compound, has been found in many medicinal plants. Its roles in tumor suppression are still under investigation. In the study, we mainly focused on exploring its applications in dealing with non-small cell lung cancer (NSCLC) and the underlying mechanisms. Here, we show that (-)-Guaiol significantly inhibits cell growth of NSCLC cells both in vitro and in vivo. Further high throughput analysis reveals that RAD51, a pivotal factor in homologous recombination repair, is a potential target for it. The following mechanism studies show that (-)-Guaiol is involved in cell autophagy to regulate the expression of RAD51, leading to double-strand breaks triggered cell apoptosis. Moreover, targeting RAD51, which is highly overexpressed in the lung adenocarcinoma tissues, can significantly increase the chemosensitivity of NSCLC cells to (-)-Guaiol both in vitro and in vivo. All in all, our studies provide an attractive insight in applying (-)-Guaiol into NSCLC treatments and further suggest that knockdown of oncogenic RAD51 will greatly enhance the chemosensitivity of patients with NSCLC.</description><subject>Adenocarcinoma - drug therapy</subject><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma of Lung</subject><subject>Animals</subject><subject>Antineoplastic Agents - chemistry</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Carcinoma, Non-Small-Cell Lung - drug therapy</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Cell Line, Tumor</subject><subject>DNA Breaks, Double-Stranded</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lysosomes - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Neoplasm Transplantation</subject><subject>Oncogenes</subject><subject>Rad51 Recombinase - metabolism</subject><subject>Recombination, Genetic</subject><subject>Research Paper</subject><subject>Sesquiterpenes - pharmacology</subject><issn>1949-2553</issn><issn>1949-2553</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUU1LxDAQDaKoqD_Ai-Soh2rSNk1yEcRvEATRc5jNTmukm9QkFfbfW9fvuczw3sybGR4h-5wdc9VU5UnwNmSIHeZjzkXN1sg217UuSiGq9T_1FtlL6YVNIWqpSr1JtkopmkZIvU3cYXFUXI_gQk8jdmMPGRN9OLsQnKYMM9e7vKRvDiiMOQzP0C1pDtT5-WiRWux7CkMYckguTSj1wRdpARO84vrRd9SCtxh3yUYLfcK9r7xDnq4uH89virv769vzs7vCVqLJRa3ZDOp2JrQSNTa6LFEgWKWlsFZyzeRcoqpaLWtUoDTXlZItCqWQwfRXtUNOP3WHcbbAuUWfI_RmiG4BcWkCOPOf8e7ZdOHNiIopWatJ4PBLIIbXEVM2C5c-vgGPYUyGT4cpVgrZTK38s9XGkFLE9mcNZ2blkvl1yaxcmmYO_t73M_HtSfUOTzqRXQ</recordid><startdate>20160920</startdate><enddate>20160920</enddate><creator>Yang, Qingyuan</creator><creator>Wu, Jianchun</creator><creator>Luo, Yingbin</creator><creator>Huang, Nan</creator><creator>Zhen, Ni</creator><creator>Zhou, Yun</creator><creator>Sun, Fenyong</creator><creator>Li, Zhi</creator><creator>Pan, Qiuhui</creator><creator>Li, Yan</creator><general>Impact Journals LLC</general><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160920</creationdate><title>(-)-Guaiol regulates RAD51 stability via autophagy to induce cell apoptosis in non-small cell lung cancer</title><author>Yang, Qingyuan ; Wu, Jianchun ; Luo, Yingbin ; Huang, Nan ; Zhen, Ni ; Zhou, Yun ; Sun, Fenyong ; Li, Zhi ; Pan, Qiuhui ; Li, Yan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-490ba4fb59854e6922e5eac8975cc71907d7e83f974e8a8919387fe588e0a2753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adenocarcinoma - drug therapy</topic><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma of Lung</topic><topic>Animals</topic><topic>Antineoplastic Agents - chemistry</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Carcinoma, Non-Small-Cell Lung - drug therapy</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Cell Line, Tumor</topic><topic>DNA Breaks, Double-Stranded</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lysosomes - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Neoplasm Transplantation</topic><topic>Oncogenes</topic><topic>Rad51 Recombinase - metabolism</topic><topic>Recombination, Genetic</topic><topic>Research Paper</topic><topic>Sesquiterpenes - pharmacology</topic><toplevel>online_resources</toplevel><creatorcontrib>Yang, Qingyuan</creatorcontrib><creatorcontrib>Wu, Jianchun</creatorcontrib><creatorcontrib>Luo, Yingbin</creatorcontrib><creatorcontrib>Huang, Nan</creatorcontrib><creatorcontrib>Zhen, Ni</creatorcontrib><creatorcontrib>Zhou, Yun</creatorcontrib><creatorcontrib>Sun, Fenyong</creatorcontrib><creatorcontrib>Li, Zhi</creatorcontrib><creatorcontrib>Pan, Qiuhui</creatorcontrib><creatorcontrib>Li, Yan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncotarget</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Qingyuan</au><au>Wu, Jianchun</au><au>Luo, Yingbin</au><au>Huang, Nan</au><au>Zhen, Ni</au><au>Zhou, Yun</au><au>Sun, Fenyong</au><au>Li, Zhi</au><au>Pan, Qiuhui</au><au>Li, Yan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>(-)-Guaiol regulates RAD51 stability via autophagy to induce cell apoptosis in non-small cell lung cancer</atitle><jtitle>Oncotarget</jtitle><addtitle>Oncotarget</addtitle><date>2016-09-20</date><risdate>2016</risdate><volume>7</volume><issue>38</issue><spage>62585</spage><epage>62597</epage><pages>62585-62597</pages><issn>1949-2553</issn><eissn>1949-2553</eissn><abstract>(-)-Guaiol, generally known as an antibacterial compound, has been found in many medicinal plants. Its roles in tumor suppression are still under investigation. In the study, we mainly focused on exploring its applications in dealing with non-small cell lung cancer (NSCLC) and the underlying mechanisms. Here, we show that (-)-Guaiol significantly inhibits cell growth of NSCLC cells both in vitro and in vivo. Further high throughput analysis reveals that RAD51, a pivotal factor in homologous recombination repair, is a potential target for it. The following mechanism studies show that (-)-Guaiol is involved in cell autophagy to regulate the expression of RAD51, leading to double-strand breaks triggered cell apoptosis. Moreover, targeting RAD51, which is highly overexpressed in the lung adenocarcinoma tissues, can significantly increase the chemosensitivity of NSCLC cells to (-)-Guaiol both in vitro and in vivo. All in all, our studies provide an attractive insight in applying (-)-Guaiol into NSCLC treatments and further suggest that knockdown of oncogenic RAD51 will greatly enhance the chemosensitivity of patients with NSCLC.</abstract><cop>United States</cop><pub>Impact Journals LLC</pub><pmid>27566579</pmid><doi>10.18632/oncotarget.11540</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1949-2553 |
| ispartof | Oncotarget, 2016-09, Vol.7 (38), p.62585-62597 |
| issn | 1949-2553 1949-2553 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5308748 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free E- Journals; PubMed Central Open Access |
| subjects | Adenocarcinoma - drug therapy Adenocarcinoma - metabolism Adenocarcinoma of Lung Animals Antineoplastic Agents - chemistry Apoptosis Autophagy Carcinoma, Non-Small-Cell Lung - drug therapy Carcinoma, Non-Small-Cell Lung - metabolism Cell Line, Tumor DNA Breaks, Double-Stranded Gene Expression Profiling Gene Expression Regulation, Neoplastic Humans Lung Neoplasms - drug therapy Lung Neoplasms - metabolism Lysosomes - metabolism Male Mice Mice, Nude Neoplasm Transplantation Oncogenes Rad51 Recombinase - metabolism Recombination, Genetic Research Paper Sesquiterpenes - pharmacology |
| title | (-)-Guaiol regulates RAD51 stability via autophagy to induce cell apoptosis in non-small cell lung cancer |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-06T14%3A40%3A49IST&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=(-)-Guaiol%20regulates%20RAD51%20stability%20via%20autophagy%20to%20induce%20cell%20apoptosis%20in%20non-small%20cell%20lung%20cancer&rft.jtitle=Oncotarget&rft.au=Yang,%20Qingyuan&rft.date=2016-09-20&rft.volume=7&rft.issue=38&rft.spage=62585&rft.epage=62597&rft.pages=62585-62597&rft.issn=1949-2553&rft.eissn=1949-2553&rft_id=info:doi/10.18632/oncotarget.11540&rft_dat=%3Cproquest_pubme%3E1854802576%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=1854802576&rft_id=info:pmid/27566579&rfr_iscdi=true |