Inactivated Sendai virus induces apoptosis and autophagy via the PI3K/Akt/mTOR/p70S6K pathway in human non-small cell lung cancer cells
Inactivated Sendai virus (HVJ-E) has shown potential anticancer efficacy in various cancer cells. However, the ability of HVJ-E to regulate cancer cell survival and death remains largely unknown. In the present study we first found that HVJ-E exhibited cytotoxic effects in the non-small cell lung ca...
Gespeichert in:
| Veröffentlicht in: | Biochemical and biophysical research communications 2015-09, Vol.465 (1), p.64-70 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 70 |
|---|---|
| container_issue | 1 |
| container_start_page | 64 |
| container_title | Biochemical and biophysical research communications |
| container_volume | 465 |
| creator | Zhang, Quan Zhu, Huixia Xu, Xiaoshuang Li, Lingyu Tan, Haiming Cai, Xiaoyao |
| description | Inactivated Sendai virus (HVJ-E) has shown potential anticancer efficacy in various cancer cells. However, the ability of HVJ-E to regulate cancer cell survival and death remains largely unknown. In the present study we first found that HVJ-E exhibited cytotoxic effects in the non-small cell lung cancer cell (NSCLC) line A549 and cisplatin-resistant A549 cells (A549/DDP). The suppression of cell viability was due to both the activation of caspases and the JNK and p38 MAPK signaling pathways in A549 and A549/DDP human lung cancer cells. In addition, we demonstrated that HVJ-E could induce autophagy in NSCLC cells via the PI3K/Akt/mTOR/p70S6K signaling pathway for the first time. Inhibiting autophagy in A549/DDP cells and inducing autophagy in A549 cells enhanced HVJ-E-induced apoptosis. These findings provide a molecular basis of HVJ-E-mediated cell death and support the notion that combination treatment with autophagy modulators is an effective strategy to augment the cytotoxic effects of HVJ-E in NSCLC cells.
•HVJ-E induces both apoptosis and autophagy in NSCLC cells.•HVJ-E-induced autophagy in NSCLC cells is associated with the PI3K/Akt/mTOR/p70S6K pathway.•Inhibiting autophagy in A549/DDP cells or inducing autophagy in A549 cells enhances HVJ-E-mediated apoptosis. |
| doi_str_mv | 10.1016/j.bbrc.2015.07.130 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1722171755</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0006291X15303612</els_id><sourcerecordid>1722171755</sourcerecordid><originalsourceid>FETCH-LOGICAL-c525t-a14938a982d0f5c1f6c88b061962a67c1d3885e3c65409bfd2f0eea7cf43658c3</originalsourceid><addsrcrecordid>eNqNkc9u1DAQhy0EokvLC3BAPnJJduzEfyJxqSooq1YqaovEzXJsp-tl4wTb2WqfgNcm2y0cERePNfrmp9F8CL0jUBIgfLkp2zaakgJhJYiSVPACLQg0UFAC9Uu0AABe0IZ8P0FvUtoAEFLz5jU6oZxWTIpqgX6tgjbZ73R2Ft-5YLXHOx-nhH2wk3EJ63EY85D8_AsW6ykP41o_7GdK47x2-Ouqulqe_8jL_v7mdjkKuONXeNR5_aj3cwheT70OOAyhSL3ebrFx87OdwgM2OhgXnxrpDL3q9Da5t8_1FH37_On-4ktxfXO5uji_LgyjLBea1E0ldSOphY4Z0nEjZQucNJxqLgyxlZTMVYazGpq2s7QD57QwXV1xJk11ij4cc8c4_Jxcyqr36bCBDm6YkiKCUiKIYOw_UJCyEfCE0iNq4pBSdJ0ao-913CsC6uBKbdTBlTq4UiDU7Goeev-cP7W9s39H_siZgY9HwM0H2XkXVTLezTezPjqTlR38v_J_A3QnpPs</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1708897055</pqid></control><display><type>article</type><title>Inactivated Sendai virus induces apoptosis and autophagy via the PI3K/Akt/mTOR/p70S6K pathway in human non-small cell lung cancer cells</title><source>MEDLINE</source><source>ScienceDirect Journals (5 years ago - present)</source><creator>Zhang, Quan ; Zhu, Huixia ; Xu, Xiaoshuang ; Li, Lingyu ; Tan, Haiming ; Cai, Xiaoyao</creator><creatorcontrib>Zhang, Quan ; Zhu, Huixia ; Xu, Xiaoshuang ; Li, Lingyu ; Tan, Haiming ; Cai, Xiaoyao</creatorcontrib><description>Inactivated Sendai virus (HVJ-E) has shown potential anticancer efficacy in various cancer cells. However, the ability of HVJ-E to regulate cancer cell survival and death remains largely unknown. In the present study we first found that HVJ-E exhibited cytotoxic effects in the non-small cell lung cancer cell (NSCLC) line A549 and cisplatin-resistant A549 cells (A549/DDP). The suppression of cell viability was due to both the activation of caspases and the JNK and p38 MAPK signaling pathways in A549 and A549/DDP human lung cancer cells. In addition, we demonstrated that HVJ-E could induce autophagy in NSCLC cells via the PI3K/Akt/mTOR/p70S6K signaling pathway for the first time. Inhibiting autophagy in A549/DDP cells and inducing autophagy in A549 cells enhanced HVJ-E-induced apoptosis. These findings provide a molecular basis of HVJ-E-mediated cell death and support the notion that combination treatment with autophagy modulators is an effective strategy to augment the cytotoxic effects of HVJ-E in NSCLC cells.
•HVJ-E induces both apoptosis and autophagy in NSCLC cells.•HVJ-E-induced autophagy in NSCLC cells is associated with the PI3K/Akt/mTOR/p70S6K pathway.•Inhibiting autophagy in A549/DDP cells or inducing autophagy in A549 cells enhances HVJ-E-mediated apoptosis.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2015.07.130</identifier><identifier>PMID: 26235873</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Antineoplastic Agents - pharmacology ; Apoptosis ; Apoptosis - genetics ; Autophagy ; Autophagy - genetics ; Cell Line, Tumor ; Cisplatin - pharmacology ; Drug Resistance, Neoplasm ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Epithelial Cells - pathology ; Epithelial Cells - virology ; Gene Expression Regulation, Neoplastic ; Humans ; Inactivated Sendai virus (HVJ-E) ; MAP Kinase Kinase 4 - genetics ; MAP Kinase Kinase 4 - metabolism ; p38 Mitogen-Activated Protein Kinases - genetics ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; PI3K/AKT/mTOR/p70S6K ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Respiratory Mucosa - drug effects ; Respiratory Mucosa - metabolism ; Respiratory Mucosa - pathology ; Respiratory Mucosa - virology ; Ribosomal Protein S6 Kinases, 70-kDa - genetics ; Ribosomal Protein S6 Kinases, 70-kDa - metabolism ; Sendai virus ; Sendai virus - chemistry ; Signal Transduction ; TOR Serine-Threonine Kinases - genetics ; TOR Serine-Threonine Kinases - metabolism ; Virus Inactivation</subject><ispartof>Biochemical and biophysical research communications, 2015-09, Vol.465 (1), p.64-70</ispartof><rights>2015 Elsevier Inc.</rights><rights>Copyright © 2015 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-a14938a982d0f5c1f6c88b061962a67c1d3885e3c65409bfd2f0eea7cf43658c3</citedby><cites>FETCH-LOGICAL-c525t-a14938a982d0f5c1f6c88b061962a67c1d3885e3c65409bfd2f0eea7cf43658c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2015.07.130$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26235873$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Quan</creatorcontrib><creatorcontrib>Zhu, Huixia</creatorcontrib><creatorcontrib>Xu, Xiaoshuang</creatorcontrib><creatorcontrib>Li, Lingyu</creatorcontrib><creatorcontrib>Tan, Haiming</creatorcontrib><creatorcontrib>Cai, Xiaoyao</creatorcontrib><title>Inactivated Sendai virus induces apoptosis and autophagy via the PI3K/Akt/mTOR/p70S6K pathway in human non-small cell lung cancer cells</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Inactivated Sendai virus (HVJ-E) has shown potential anticancer efficacy in various cancer cells. However, the ability of HVJ-E to regulate cancer cell survival and death remains largely unknown. In the present study we first found that HVJ-E exhibited cytotoxic effects in the non-small cell lung cancer cell (NSCLC) line A549 and cisplatin-resistant A549 cells (A549/DDP). The suppression of cell viability was due to both the activation of caspases and the JNK and p38 MAPK signaling pathways in A549 and A549/DDP human lung cancer cells. In addition, we demonstrated that HVJ-E could induce autophagy in NSCLC cells via the PI3K/Akt/mTOR/p70S6K signaling pathway for the first time. Inhibiting autophagy in A549/DDP cells and inducing autophagy in A549 cells enhanced HVJ-E-induced apoptosis. These findings provide a molecular basis of HVJ-E-mediated cell death and support the notion that combination treatment with autophagy modulators is an effective strategy to augment the cytotoxic effects of HVJ-E in NSCLC cells.
•HVJ-E induces both apoptosis and autophagy in NSCLC cells.•HVJ-E-induced autophagy in NSCLC cells is associated with the PI3K/Akt/mTOR/p70S6K pathway.•Inhibiting autophagy in A549/DDP cells or inducing autophagy in A549 cells enhances HVJ-E-mediated apoptosis.</description><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Autophagy</subject><subject>Autophagy - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cisplatin - pharmacology</subject><subject>Drug Resistance, Neoplasm</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - pathology</subject><subject>Epithelial Cells - virology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Inactivated Sendai virus (HVJ-E)</subject><subject>MAP Kinase Kinase 4 - genetics</subject><subject>MAP Kinase Kinase 4 - metabolism</subject><subject>p38 Mitogen-Activated Protein Kinases - genetics</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>PI3K/AKT/mTOR/p70S6K</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Respiratory Mucosa - drug effects</subject><subject>Respiratory Mucosa - metabolism</subject><subject>Respiratory Mucosa - pathology</subject><subject>Respiratory Mucosa - virology</subject><subject>Ribosomal Protein S6 Kinases, 70-kDa - genetics</subject><subject>Ribosomal Protein S6 Kinases, 70-kDa - metabolism</subject><subject>Sendai virus</subject><subject>Sendai virus - chemistry</subject><subject>Signal Transduction</subject><subject>TOR Serine-Threonine Kinases - genetics</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Virus Inactivation</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc9u1DAQhy0EokvLC3BAPnJJduzEfyJxqSooq1YqaovEzXJsp-tl4wTb2WqfgNcm2y0cERePNfrmp9F8CL0jUBIgfLkp2zaakgJhJYiSVPACLQg0UFAC9Uu0AABe0IZ8P0FvUtoAEFLz5jU6oZxWTIpqgX6tgjbZ73R2Ft-5YLXHOx-nhH2wk3EJ63EY85D8_AsW6ykP41o_7GdK47x2-Ouqulqe_8jL_v7mdjkKuONXeNR5_aj3cwheT70OOAyhSL3ebrFx87OdwgM2OhgXnxrpDL3q9Da5t8_1FH37_On-4ktxfXO5uji_LgyjLBea1E0ldSOphY4Z0nEjZQucNJxqLgyxlZTMVYazGpq2s7QD57QwXV1xJk11ij4cc8c4_Jxcyqr36bCBDm6YkiKCUiKIYOw_UJCyEfCE0iNq4pBSdJ0ao-913CsC6uBKbdTBlTq4UiDU7Goeev-cP7W9s39H_siZgY9HwM0H2XkXVTLezTezPjqTlR38v_J_A3QnpPs</recordid><startdate>20150911</startdate><enddate>20150911</enddate><creator>Zhang, Quan</creator><creator>Zhu, Huixia</creator><creator>Xu, Xiaoshuang</creator><creator>Li, Lingyu</creator><creator>Tan, Haiming</creator><creator>Cai, Xiaoyao</creator><general>Elsevier Inc</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>7U9</scope><scope>H94</scope></search><sort><creationdate>20150911</creationdate><title>Inactivated Sendai virus induces apoptosis and autophagy via the PI3K/Akt/mTOR/p70S6K pathway in human non-small cell lung cancer cells</title><author>Zhang, Quan ; Zhu, Huixia ; Xu, Xiaoshuang ; Li, Lingyu ; Tan, Haiming ; Cai, Xiaoyao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c525t-a14938a982d0f5c1f6c88b061962a67c1d3885e3c65409bfd2f0eea7cf43658c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Autophagy</topic><topic>Autophagy - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cisplatin - pharmacology</topic><topic>Drug Resistance, Neoplasm</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelial Cells - pathology</topic><topic>Epithelial Cells - virology</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Inactivated Sendai virus (HVJ-E)</topic><topic>MAP Kinase Kinase 4 - genetics</topic><topic>MAP Kinase Kinase 4 - metabolism</topic><topic>p38 Mitogen-Activated Protein Kinases - genetics</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>PI3K/AKT/mTOR/p70S6K</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Respiratory Mucosa - drug effects</topic><topic>Respiratory Mucosa - metabolism</topic><topic>Respiratory Mucosa - pathology</topic><topic>Respiratory Mucosa - virology</topic><topic>Ribosomal Protein S6 Kinases, 70-kDa - genetics</topic><topic>Ribosomal Protein S6 Kinases, 70-kDa - metabolism</topic><topic>Sendai virus</topic><topic>Sendai virus - chemistry</topic><topic>Signal Transduction</topic><topic>TOR Serine-Threonine Kinases - genetics</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Virus Inactivation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Quan</creatorcontrib><creatorcontrib>Zhu, Huixia</creatorcontrib><creatorcontrib>Xu, Xiaoshuang</creatorcontrib><creatorcontrib>Li, Lingyu</creatorcontrib><creatorcontrib>Tan, Haiming</creatorcontrib><creatorcontrib>Cai, Xiaoyao</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>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Quan</au><au>Zhu, Huixia</au><au>Xu, Xiaoshuang</au><au>Li, Lingyu</au><au>Tan, Haiming</au><au>Cai, Xiaoyao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inactivated Sendai virus induces apoptosis and autophagy via the PI3K/Akt/mTOR/p70S6K pathway in human non-small cell lung cancer cells</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2015-09-11</date><risdate>2015</risdate><volume>465</volume><issue>1</issue><spage>64</spage><epage>70</epage><pages>64-70</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Inactivated Sendai virus (HVJ-E) has shown potential anticancer efficacy in various cancer cells. However, the ability of HVJ-E to regulate cancer cell survival and death remains largely unknown. In the present study we first found that HVJ-E exhibited cytotoxic effects in the non-small cell lung cancer cell (NSCLC) line A549 and cisplatin-resistant A549 cells (A549/DDP). The suppression of cell viability was due to both the activation of caspases and the JNK and p38 MAPK signaling pathways in A549 and A549/DDP human lung cancer cells. In addition, we demonstrated that HVJ-E could induce autophagy in NSCLC cells via the PI3K/Akt/mTOR/p70S6K signaling pathway for the first time. Inhibiting autophagy in A549/DDP cells and inducing autophagy in A549 cells enhanced HVJ-E-induced apoptosis. These findings provide a molecular basis of HVJ-E-mediated cell death and support the notion that combination treatment with autophagy modulators is an effective strategy to augment the cytotoxic effects of HVJ-E in NSCLC cells.
•HVJ-E induces both apoptosis and autophagy in NSCLC cells.•HVJ-E-induced autophagy in NSCLC cells is associated with the PI3K/Akt/mTOR/p70S6K pathway.•Inhibiting autophagy in A549/DDP cells or inducing autophagy in A549 cells enhances HVJ-E-mediated apoptosis.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26235873</pmid><doi>10.1016/j.bbrc.2015.07.130</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0006-291X |
| ispartof | Biochemical and biophysical research communications, 2015-09, Vol.465 (1), p.64-70 |
| issn | 0006-291X 1090-2104 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1722171755 |
| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Antineoplastic Agents - pharmacology Apoptosis Apoptosis - genetics Autophagy Autophagy - genetics Cell Line, Tumor Cisplatin - pharmacology Drug Resistance, Neoplasm Epithelial Cells - drug effects Epithelial Cells - metabolism Epithelial Cells - pathology Epithelial Cells - virology Gene Expression Regulation, Neoplastic Humans Inactivated Sendai virus (HVJ-E) MAP Kinase Kinase 4 - genetics MAP Kinase Kinase 4 - metabolism p38 Mitogen-Activated Protein Kinases - genetics p38 Mitogen-Activated Protein Kinases - metabolism Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism PI3K/AKT/mTOR/p70S6K Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Respiratory Mucosa - drug effects Respiratory Mucosa - metabolism Respiratory Mucosa - pathology Respiratory Mucosa - virology Ribosomal Protein S6 Kinases, 70-kDa - genetics Ribosomal Protein S6 Kinases, 70-kDa - metabolism Sendai virus Sendai virus - chemistry Signal Transduction TOR Serine-Threonine Kinases - genetics TOR Serine-Threonine Kinases - metabolism Virus Inactivation |
| title | Inactivated Sendai virus induces apoptosis and autophagy via the PI3K/Akt/mTOR/p70S6K pathway in human non-small cell lung cancer cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T23%3A22%3A19IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Inactivated%20Sendai%20virus%20induces%20apoptosis%20and%20autophagy%20via%20the%20PI3K/Akt/mTOR/p70S6K%20pathway%20in%20human%20non-small%20cell%20lung%20cancer%20cells&rft.jtitle=Biochemical%20and%20biophysical%20research%20communications&rft.au=Zhang,%20Quan&rft.date=2015-09-11&rft.volume=465&rft.issue=1&rft.spage=64&rft.epage=70&rft.pages=64-70&rft.issn=0006-291X&rft.eissn=1090-2104&rft_id=info:doi/10.1016/j.bbrc.2015.07.130&rft_dat=%3Cproquest_cross%3E1722171755%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1708897055&rft_id=info:pmid/26235873&rft_els_id=S0006291X15303612&rfr_iscdi=true |