Ophiopogonin B-induced autophagy in non-small cell lung cancer cells via inhibition of the PI3K/Akt signaling pathway
Ophiopogonin B (OP-B) is a bioactive component of Radix Ophiopogon Japonicus, which is often used in Chinese traditional medicine to treat pulmonary disease. However, whether or not OP-B has any potential antitumor activity has not been reported. Here, we show that the non-small cell lung cancer (NS...
Gespeichert in:
| Veröffentlicht in: | Oncology reports 2013-02, Vol.29 (2), p.430-436 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 436 |
|---|---|
| container_issue | 2 |
| container_start_page | 430 |
| container_title | Oncology reports |
| container_volume | 29 |
| creator | CHEN, MEIJUAN DU, YUHONG QUI, MIN WANG, MINGYAN CHEN, KEJUN HUANG, ZHENZHOU JIANG, MIAO XIONG, FEI CHEN, JIANPING ZHOU, JING JIANG, FENGRONG YIN, LIAN TANG, YUPING YE, LIHONG ZHAN, ZHEN DUAN, JIN-AO FU, HAI-AN ZHANG, XU |
| description | Ophiopogonin B (OP-B) is a bioactive component of Radix Ophiopogon Japonicus, which is often used in Chinese traditional medicine to treat pulmonary disease. However, whether or not OP-B has any potential antitumor activity has not been reported. Here, we show that the non-small cell lung cancer (NSCLC) cell lines NCI-H157 and NCI-H460 treated with OP-B grow more slowly and accumulate vacuoles in their cytoplasm compared to untreated control cells. Flow cytometric analysis showed that the cells were arrested in G0/G1 phase. Nuclear morphology, Annexin-V/PI staining, and expression of cleaved caspase-3 all confirm that OP-B does not induce apoptosis. Instead, based on results from both transmission electron microscopy (TEM) and the expression of microtubule-associated protein 1 light chain 3-II (LC3-II), we determined that OP-B treatment induced autophagy in both cell lines. Next, we examined the PI3K/Akt/mTOR signaling pathway and found that OP-B inhibited phosphorylation of Akt (Ser473, Thr308) in NCI-H157 cells and also inhibited several key components of the pathway in NCI-H460 cells, such as p-Akt(Ser473, Thr308), p-p70S6K (Thr389). Additionally, insulin-mediated activation of the PI3K/Akt/mTOR pathway provides evidence that activation of this pathway may correlate with induction of autophagy in H460 cells. Therefore, OP-B is a prospective inhibitor of PI3K/Akt and may be used as an alternative compound to treat NSCLC. |
| doi_str_mv | 10.3892/or.2012.2131 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3583607</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1932668346</sourcerecordid><originalsourceid>FETCH-LOGICAL-c443t-2a813ba457e98cac6809e6b9a30b54855fe76b582d657e38fe1aecc8add141ed3</originalsourceid><addsrcrecordid>eNpdkUtv1TAQhSMEoqWwY40sISEW-NavOPYGqVQ8KiqVBUjsrInjJC65drCTovvv8eWW8th4rJnPR3N8quopJRuuNDuNacMIZRtGOb1XHdNGU8wEp_fLnTCKOa-_HlWPcr4mhDVE6ofVEeO0ppqo42q9mkcf5zjE4AN6g33oVus6BOsS5xGGHSrtEAPOW5gmZF05pjUMyEKwLv1qZHTjoXCjb_3iY0CxR8vo0KcL_vH07NuCsh8CTL68mmEZf8DucfWghym7J7f1pPry7u3n8w_48ur9xfnZJbZC8AUzUJS3IOrGaWXBSkW0k60GTtpaqLruXSPbWrFOFoSr3lFw1iroOiqo6_hJ9fqgO6_t1nXWhSXBZObkt5B2JoI3_06CH80QbwyvFZekKQIvbwVS_L66vJitz3vPEFxcs6FMlD8mWpCCPv8PvY5rKr4LpTmTUnEhC_XqQNkUc06uv1uGErPP08Rk9nmafZ4Ff_a3gTv4d4AFeHEA8gyh813Mf9wlzDQmDBPBCf8Jc5yplw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1932668346</pqid></control><display><type>article</type><title>Ophiopogonin B-induced autophagy in non-small cell lung cancer cells via inhibition of the PI3K/Akt signaling pathway</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>CHEN, MEIJUAN ; DU, YUHONG ; QUI, MIN ; WANG, MINGYAN ; CHEN, KEJUN ; HUANG, ZHENZHOU ; JIANG, MIAO ; XIONG, FEI ; CHEN, JIANPING ; ZHOU, JING ; JIANG, FENGRONG ; YIN, LIAN ; TANG, YUPING ; YE, LIHONG ; ZHAN, ZHEN ; DUAN, JIN-AO ; FU, HAI-AN ; ZHANG, XU</creator><creatorcontrib>CHEN, MEIJUAN ; DU, YUHONG ; QUI, MIN ; WANG, MINGYAN ; CHEN, KEJUN ; HUANG, ZHENZHOU ; JIANG, MIAO ; XIONG, FEI ; CHEN, JIANPING ; ZHOU, JING ; JIANG, FENGRONG ; YIN, LIAN ; TANG, YUPING ; YE, LIHONG ; ZHAN, ZHEN ; DUAN, JIN-AO ; FU, HAI-AN ; ZHANG, XU</creatorcontrib><description>Ophiopogonin B (OP-B) is a bioactive component of Radix Ophiopogon Japonicus, which is often used in Chinese traditional medicine to treat pulmonary disease. However, whether or not OP-B has any potential antitumor activity has not been reported. Here, we show that the non-small cell lung cancer (NSCLC) cell lines NCI-H157 and NCI-H460 treated with OP-B grow more slowly and accumulate vacuoles in their cytoplasm compared to untreated control cells. Flow cytometric analysis showed that the cells were arrested in G0/G1 phase. Nuclear morphology, Annexin-V/PI staining, and expression of cleaved caspase-3 all confirm that OP-B does not induce apoptosis. Instead, based on results from both transmission electron microscopy (TEM) and the expression of microtubule-associated protein 1 light chain 3-II (LC3-II), we determined that OP-B treatment induced autophagy in both cell lines. Next, we examined the PI3K/Akt/mTOR signaling pathway and found that OP-B inhibited phosphorylation of Akt (Ser473, Thr308) in NCI-H157 cells and also inhibited several key components of the pathway in NCI-H460 cells, such as p-Akt(Ser473, Thr308), p-p70S6K (Thr389). Additionally, insulin-mediated activation of the PI3K/Akt/mTOR pathway provides evidence that activation of this pathway may correlate with induction of autophagy in H460 cells. Therefore, OP-B is a prospective inhibitor of PI3K/Akt and may be used as an alternative compound to treat NSCLC.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2012.2131</identifier><identifier>PMID: 23151908</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Apoptosis ; Autophagy ; Autophagy - drug effects ; Carcinoma, Non-Small-Cell Lung - drug therapy ; Carcinoma, Non-Small-Cell Lung - enzymology ; Cell cycle ; Cell Cycle Checkpoints - drug effects ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cytoplasm ; Humans ; Kinases ; Lung cancer ; Lung Neoplasms - drug therapy ; Lung Neoplasms - enzymology ; Microtubule-Associated Proteins - metabolism ; Morphology ; natural medicines ; non-small cell lung cancer ; Ophiopogonin B ; Phosphatidylinositol 3-Kinases - metabolism ; PI3K/Akt/mTOR ; Plant Extracts - pharmacology ; Proto-Oncogene Proteins c-akt - metabolism ; Saponins - pharmacology ; Signal Transduction - drug effects ; Spirostans - pharmacology ; Vacuoles - drug effects</subject><ispartof>Oncology reports, 2013-02, Vol.29 (2), p.430-436</ispartof><rights>Copyright © 2013, Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2013</rights><rights>Copyright © 2013, Spandidos Publications 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c443t-2a813ba457e98cac6809e6b9a30b54855fe76b582d657e38fe1aecc8add141ed3</citedby><cites>FETCH-LOGICAL-c443t-2a813ba457e98cac6809e6b9a30b54855fe76b582d657e38fe1aecc8add141ed3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23151908$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CHEN, MEIJUAN</creatorcontrib><creatorcontrib>DU, YUHONG</creatorcontrib><creatorcontrib>QUI, MIN</creatorcontrib><creatorcontrib>WANG, MINGYAN</creatorcontrib><creatorcontrib>CHEN, KEJUN</creatorcontrib><creatorcontrib>HUANG, ZHENZHOU</creatorcontrib><creatorcontrib>JIANG, MIAO</creatorcontrib><creatorcontrib>XIONG, FEI</creatorcontrib><creatorcontrib>CHEN, JIANPING</creatorcontrib><creatorcontrib>ZHOU, JING</creatorcontrib><creatorcontrib>JIANG, FENGRONG</creatorcontrib><creatorcontrib>YIN, LIAN</creatorcontrib><creatorcontrib>TANG, YUPING</creatorcontrib><creatorcontrib>YE, LIHONG</creatorcontrib><creatorcontrib>ZHAN, ZHEN</creatorcontrib><creatorcontrib>DUAN, JIN-AO</creatorcontrib><creatorcontrib>FU, HAI-AN</creatorcontrib><creatorcontrib>ZHANG, XU</creatorcontrib><title>Ophiopogonin B-induced autophagy in non-small cell lung cancer cells via inhibition of the PI3K/Akt signaling pathway</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Ophiopogonin B (OP-B) is a bioactive component of Radix Ophiopogon Japonicus, which is often used in Chinese traditional medicine to treat pulmonary disease. However, whether or not OP-B has any potential antitumor activity has not been reported. Here, we show that the non-small cell lung cancer (NSCLC) cell lines NCI-H157 and NCI-H460 treated with OP-B grow more slowly and accumulate vacuoles in their cytoplasm compared to untreated control cells. Flow cytometric analysis showed that the cells were arrested in G0/G1 phase. Nuclear morphology, Annexin-V/PI staining, and expression of cleaved caspase-3 all confirm that OP-B does not induce apoptosis. Instead, based on results from both transmission electron microscopy (TEM) and the expression of microtubule-associated protein 1 light chain 3-II (LC3-II), we determined that OP-B treatment induced autophagy in both cell lines. Next, we examined the PI3K/Akt/mTOR signaling pathway and found that OP-B inhibited phosphorylation of Akt (Ser473, Thr308) in NCI-H157 cells and also inhibited several key components of the pathway in NCI-H460 cells, such as p-Akt(Ser473, Thr308), p-p70S6K (Thr389). Additionally, insulin-mediated activation of the PI3K/Akt/mTOR pathway provides evidence that activation of this pathway may correlate with induction of autophagy in H460 cells. Therefore, OP-B is a prospective inhibitor of PI3K/Akt and may be used as an alternative compound to treat NSCLC.</description><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Carcinoma, Non-Small-Cell Lung - drug therapy</subject><subject>Carcinoma, Non-Small-Cell Lung - enzymology</subject><subject>Cell cycle</subject><subject>Cell Cycle Checkpoints - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cytoplasm</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - enzymology</subject><subject>Microtubule-Associated Proteins - metabolism</subject><subject>Morphology</subject><subject>natural medicines</subject><subject>non-small cell lung cancer</subject><subject>Ophiopogonin B</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>PI3K/Akt/mTOR</subject><subject>Plant Extracts - pharmacology</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Saponins - pharmacology</subject><subject>Signal Transduction - drug effects</subject><subject>Spirostans - pharmacology</subject><subject>Vacuoles - drug effects</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpdkUtv1TAQhSMEoqWwY40sISEW-NavOPYGqVQ8KiqVBUjsrInjJC65drCTovvv8eWW8th4rJnPR3N8quopJRuuNDuNacMIZRtGOb1XHdNGU8wEp_fLnTCKOa-_HlWPcr4mhDVE6ofVEeO0ppqo42q9mkcf5zjE4AN6g33oVus6BOsS5xGGHSrtEAPOW5gmZF05pjUMyEKwLv1qZHTjoXCjb_3iY0CxR8vo0KcL_vH07NuCsh8CTL68mmEZf8DucfWghym7J7f1pPry7u3n8w_48ur9xfnZJbZC8AUzUJS3IOrGaWXBSkW0k60GTtpaqLruXSPbWrFOFoSr3lFw1iroOiqo6_hJ9fqgO6_t1nXWhSXBZObkt5B2JoI3_06CH80QbwyvFZekKQIvbwVS_L66vJitz3vPEFxcs6FMlD8mWpCCPv8PvY5rKr4LpTmTUnEhC_XqQNkUc06uv1uGErPP08Rk9nmafZ4Ff_a3gTv4d4AFeHEA8gyh813Mf9wlzDQmDBPBCf8Jc5yplw</recordid><startdate>20130201</startdate><enddate>20130201</enddate><creator>CHEN, MEIJUAN</creator><creator>DU, YUHONG</creator><creator>QUI, MIN</creator><creator>WANG, MINGYAN</creator><creator>CHEN, KEJUN</creator><creator>HUANG, ZHENZHOU</creator><creator>JIANG, MIAO</creator><creator>XIONG, FEI</creator><creator>CHEN, JIANPING</creator><creator>ZHOU, JING</creator><creator>JIANG, FENGRONG</creator><creator>YIN, LIAN</creator><creator>TANG, YUPING</creator><creator>YE, LIHONG</creator><creator>ZHAN, ZHEN</creator><creator>DUAN, JIN-AO</creator><creator>FU, HAI-AN</creator><creator>ZHANG, XU</creator><general>D.A. Spandidos</general><general>Spandidos Publications UK Ltd</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20130201</creationdate><title>Ophiopogonin B-induced autophagy in non-small cell lung cancer cells via inhibition of the PI3K/Akt signaling pathway</title><author>CHEN, MEIJUAN ; DU, YUHONG ; QUI, MIN ; WANG, MINGYAN ; CHEN, KEJUN ; HUANG, ZHENZHOU ; JIANG, MIAO ; XIONG, FEI ; CHEN, JIANPING ; ZHOU, JING ; JIANG, FENGRONG ; YIN, LIAN ; TANG, YUPING ; YE, LIHONG ; ZHAN, ZHEN ; DUAN, JIN-AO ; FU, HAI-AN ; ZHANG, XU</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c443t-2a813ba457e98cac6809e6b9a30b54855fe76b582d657e38fe1aecc8add141ed3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Autophagy - drug effects</topic><topic>Carcinoma, Non-Small-Cell Lung - drug therapy</topic><topic>Carcinoma, Non-Small-Cell Lung - enzymology</topic><topic>Cell cycle</topic><topic>Cell Cycle Checkpoints - drug effects</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Cytoplasm</topic><topic>Humans</topic><topic>Kinases</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - enzymology</topic><topic>Microtubule-Associated Proteins - metabolism</topic><topic>Morphology</topic><topic>natural medicines</topic><topic>non-small cell lung cancer</topic><topic>Ophiopogonin B</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>PI3K/Akt/mTOR</topic><topic>Plant Extracts - pharmacology</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Saponins - pharmacology</topic><topic>Signal Transduction - drug effects</topic><topic>Spirostans - pharmacology</topic><topic>Vacuoles - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CHEN, MEIJUAN</creatorcontrib><creatorcontrib>DU, YUHONG</creatorcontrib><creatorcontrib>QUI, MIN</creatorcontrib><creatorcontrib>WANG, MINGYAN</creatorcontrib><creatorcontrib>CHEN, KEJUN</creatorcontrib><creatorcontrib>HUANG, ZHENZHOU</creatorcontrib><creatorcontrib>JIANG, MIAO</creatorcontrib><creatorcontrib>XIONG, FEI</creatorcontrib><creatorcontrib>CHEN, JIANPING</creatorcontrib><creatorcontrib>ZHOU, JING</creatorcontrib><creatorcontrib>JIANG, FENGRONG</creatorcontrib><creatorcontrib>YIN, LIAN</creatorcontrib><creatorcontrib>TANG, YUPING</creatorcontrib><creatorcontrib>YE, LIHONG</creatorcontrib><creatorcontrib>ZHAN, ZHEN</creatorcontrib><creatorcontrib>DUAN, JIN-AO</creatorcontrib><creatorcontrib>FU, HAI-AN</creatorcontrib><creatorcontrib>ZHANG, XU</creatorcontrib><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>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CHEN, MEIJUAN</au><au>DU, YUHONG</au><au>QUI, MIN</au><au>WANG, MINGYAN</au><au>CHEN, KEJUN</au><au>HUANG, ZHENZHOU</au><au>JIANG, MIAO</au><au>XIONG, FEI</au><au>CHEN, JIANPING</au><au>ZHOU, JING</au><au>JIANG, FENGRONG</au><au>YIN, LIAN</au><au>TANG, YUPING</au><au>YE, LIHONG</au><au>ZHAN, ZHEN</au><au>DUAN, JIN-AO</au><au>FU, HAI-AN</au><au>ZHANG, XU</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ophiopogonin B-induced autophagy in non-small cell lung cancer cells via inhibition of the PI3K/Akt signaling pathway</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2013-02-01</date><risdate>2013</risdate><volume>29</volume><issue>2</issue><spage>430</spage><epage>436</epage><pages>430-436</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Ophiopogonin B (OP-B) is a bioactive component of Radix Ophiopogon Japonicus, which is often used in Chinese traditional medicine to treat pulmonary disease. However, whether or not OP-B has any potential antitumor activity has not been reported. Here, we show that the non-small cell lung cancer (NSCLC) cell lines NCI-H157 and NCI-H460 treated with OP-B grow more slowly and accumulate vacuoles in their cytoplasm compared to untreated control cells. Flow cytometric analysis showed that the cells were arrested in G0/G1 phase. Nuclear morphology, Annexin-V/PI staining, and expression of cleaved caspase-3 all confirm that OP-B does not induce apoptosis. Instead, based on results from both transmission electron microscopy (TEM) and the expression of microtubule-associated protein 1 light chain 3-II (LC3-II), we determined that OP-B treatment induced autophagy in both cell lines. Next, we examined the PI3K/Akt/mTOR signaling pathway and found that OP-B inhibited phosphorylation of Akt (Ser473, Thr308) in NCI-H157 cells and also inhibited several key components of the pathway in NCI-H460 cells, such as p-Akt(Ser473, Thr308), p-p70S6K (Thr389). Additionally, insulin-mediated activation of the PI3K/Akt/mTOR pathway provides evidence that activation of this pathway may correlate with induction of autophagy in H460 cells. Therefore, OP-B is a prospective inhibitor of PI3K/Akt and may be used as an alternative compound to treat NSCLC.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>23151908</pmid><doi>10.3892/or.2012.2131</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1021-335X |
| ispartof | Oncology reports, 2013-02, Vol.29 (2), p.430-436 |
| issn | 1021-335X 1791-2431 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3583607 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Apoptosis Autophagy Autophagy - drug effects Carcinoma, Non-Small-Cell Lung - drug therapy Carcinoma, Non-Small-Cell Lung - enzymology Cell cycle Cell Cycle Checkpoints - drug effects Cell Line, Tumor Cell Proliferation - drug effects Cytoplasm Humans Kinases Lung cancer Lung Neoplasms - drug therapy Lung Neoplasms - enzymology Microtubule-Associated Proteins - metabolism Morphology natural medicines non-small cell lung cancer Ophiopogonin B Phosphatidylinositol 3-Kinases - metabolism PI3K/Akt/mTOR Plant Extracts - pharmacology Proto-Oncogene Proteins c-akt - metabolism Saponins - pharmacology Signal Transduction - drug effects Spirostans - pharmacology Vacuoles - drug effects |
| title | Ophiopogonin B-induced autophagy in non-small cell lung cancer cells via inhibition of the PI3K/Akt signaling pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-22T19%3A53%3A17IST&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=Ophiopogonin%20B-induced%20autophagy%20in%20non-small%20cell%20lung%20cancer%20cells%20via%20inhibition%20of%20the%20PI3K/Akt%20signaling%20pathway&rft.jtitle=Oncology%20reports&rft.au=CHEN,%20MEIJUAN&rft.date=2013-02-01&rft.volume=29&rft.issue=2&rft.spage=430&rft.epage=436&rft.pages=430-436&rft.issn=1021-335X&rft.eissn=1791-2431&rft_id=info:doi/10.3892/or.2012.2131&rft_dat=%3Cproquest_pubme%3E1932668346%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=1932668346&rft_id=info:pmid/23151908&rfr_iscdi=true |