EVA1A inhibits GBM cell proliferation by inducing autophagy and apoptosis
Eva-1 homolog A (EVA1A) is a novel lysosome and endoplasmic reticulum-associated protein involved in autophagy and apoptosis. In this study, we constructed a recombinant adenovirus 5-EVA1A vector (Ad5-EVA1A) to overexpress EVA1A in glioblastoma (GBM) cell lines and evaluated its anti-tumor activitie...
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| Veröffentlicht in: | Experimental cell research 2017-03, Vol.352 (1), p.130-138 |
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| creator | Shen, Xue Kan, Shifeng Liu, Zhen Lu, Guang Zhang, Xiaoyan Chen, Yingyu Bai, Yun |
| description | Eva-1 homolog A (EVA1A) is a novel lysosome and endoplasmic reticulum-associated protein involved in autophagy and apoptosis. In this study, we constructed a recombinant adenovirus 5-EVA1A vector (Ad5-EVA1A) to overexpress EVA1A in glioblastoma (GBM) cell lines and evaluated its anti-tumor activities in vitro and in vivo. We found that overexpression of EVA1A in three GBM cell lines (U251, U87 and SHG44) resulted in a suppression of tumor cell growth via activation of autophagy and induction of cell apoptosis in a dose- and time-dependent manner. EVA1A-mediated autophagy was associated with inactivation of the mTOR/RPS6KB1 signaling pathway. Furthermore in vivo, overexpression of EVA1A successfully inhibited tumor growth in NOD/SCID mice. Our data suggest that EVA1A-induced autophagy and apoptosis play a role in suppressing the development of GBM and their up-regulation may be an effective method for treating this form of cancer.
•Overexpression of EVA1A suppresses GBM cell growth.•EVA1A induces autophagy through the mTOR/RPS6KB1 pathway.•EVA1A induces GBM cell apoptosis.•EVA1A inhibits the development of GBM in vivo. |
| doi_str_mv | 10.1016/j.yexcr.2017.02.003 |
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•Overexpression of EVA1A suppresses GBM cell growth.•EVA1A induces autophagy through the mTOR/RPS6KB1 pathway.•EVA1A induces GBM cell apoptosis.•EVA1A inhibits the development of GBM in vivo.</description><identifier>ISSN: 0014-4827</identifier><identifier>EISSN: 1090-2422</identifier><identifier>DOI: 10.1016/j.yexcr.2017.02.003</identifier><identifier>PMID: 28185834</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; ADENOVIRUS ; Animals ; Anti-tumor activity ; APOPTOSIS ; Autophagy ; Blotting, Western ; BUDR ; Cell Adhesion Molecules - genetics ; Cell Adhesion Molecules - metabolism ; CELL PROLIFERATION ; DOSES ; ENDOPLASMIC RETICULUM ; EVA1A ; Female ; GBM ; Glioblastoma - genetics ; Glioblastoma - metabolism ; Glioblastoma - pathology ; GLIOMAS ; Humans ; IN VITRO ; IN VIVO ; INACTIVATION ; INDUCTION ; INHIBITION ; LYSOSOMES ; MICE ; Mice, Inbred NOD ; Mice, SCID ; mTOR/RPS6KB1 ; PHOSPHOTRANSFERASES ; PLANT GROWTH ; POLYPEPTIDES ; Proliferation ; Real-Time Polymerase Chain Reaction ; REGULATIONS ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; TIME DEPENDENCE ; TUMOR CELLS ; Tumor Cells, Cultured ; VECTORS ; VISIBLE RADIATION ; Xenograft Model Antitumor Assays</subject><ispartof>Experimental cell research, 2017-03, Vol.352 (1), p.130-138</ispartof><rights>2017 Elsevier Inc.</rights><rights>Copyright © 2017 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c453t-a5083392864c53e079d31c36fe50c6ec30774a12aa9c9090caef11dba2179d733</citedby><cites>FETCH-LOGICAL-c453t-a5083392864c53e079d31c36fe50c6ec30774a12aa9c9090caef11dba2179d733</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.yexcr.2017.02.003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,778,782,883,3539,27911,27912,45982</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28185834$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22649828$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Shen, Xue</creatorcontrib><creatorcontrib>Kan, Shifeng</creatorcontrib><creatorcontrib>Liu, Zhen</creatorcontrib><creatorcontrib>Lu, Guang</creatorcontrib><creatorcontrib>Zhang, Xiaoyan</creatorcontrib><creatorcontrib>Chen, Yingyu</creatorcontrib><creatorcontrib>Bai, Yun</creatorcontrib><title>EVA1A inhibits GBM cell proliferation by inducing autophagy and apoptosis</title><title>Experimental cell research</title><addtitle>Exp Cell Res</addtitle><description>Eva-1 homolog A (EVA1A) is a novel lysosome and endoplasmic reticulum-associated protein involved in autophagy and apoptosis. In this study, we constructed a recombinant adenovirus 5-EVA1A vector (Ad5-EVA1A) to overexpress EVA1A in glioblastoma (GBM) cell lines and evaluated its anti-tumor activities in vitro and in vivo. We found that overexpression of EVA1A in three GBM cell lines (U251, U87 and SHG44) resulted in a suppression of tumor cell growth via activation of autophagy and induction of cell apoptosis in a dose- and time-dependent manner. EVA1A-mediated autophagy was associated with inactivation of the mTOR/RPS6KB1 signaling pathway. Furthermore in vivo, overexpression of EVA1A successfully inhibited tumor growth in NOD/SCID mice. Our data suggest that EVA1A-induced autophagy and apoptosis play a role in suppressing the development of GBM and their up-regulation may be an effective method for treating this form of cancer.
•Overexpression of EVA1A suppresses GBM cell growth.•EVA1A induces autophagy through the mTOR/RPS6KB1 pathway.•EVA1A induces GBM cell apoptosis.•EVA1A inhibits the development of GBM in vivo.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>ADENOVIRUS</subject><subject>Animals</subject><subject>Anti-tumor activity</subject><subject>APOPTOSIS</subject><subject>Autophagy</subject><subject>Blotting, Western</subject><subject>BUDR</subject><subject>Cell Adhesion Molecules - genetics</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>CELL PROLIFERATION</subject><subject>DOSES</subject><subject>ENDOPLASMIC RETICULUM</subject><subject>EVA1A</subject><subject>Female</subject><subject>GBM</subject><subject>Glioblastoma - genetics</subject><subject>Glioblastoma - metabolism</subject><subject>Glioblastoma - pathology</subject><subject>GLIOMAS</subject><subject>Humans</subject><subject>IN VITRO</subject><subject>IN VIVO</subject><subject>INACTIVATION</subject><subject>INDUCTION</subject><subject>INHIBITION</subject><subject>LYSOSOMES</subject><subject>MICE</subject><subject>Mice, Inbred NOD</subject><subject>Mice, SCID</subject><subject>mTOR/RPS6KB1</subject><subject>PHOSPHOTRANSFERASES</subject><subject>PLANT GROWTH</subject><subject>POLYPEPTIDES</subject><subject>Proliferation</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>REGULATIONS</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>TIME DEPENDENCE</subject><subject>TUMOR CELLS</subject><subject>Tumor Cells, Cultured</subject><subject>VECTORS</subject><subject>VISIBLE RADIATION</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0014-4827</issn><issn>1090-2422</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFu1DAQhi1ERZfCEyChSFy4JJ2xncQ5cNhWpVRqxQW4Wl5n0vVqNw62g9i3x2ELx57m8s3883-MvUOoELC53FVH-m1DxQHbCngFIF6wFUIHJZecv2QrAJSlVLw9Z69j3AGAUti8YudcoaqVkCt2d_NjjevCjVu3cSkWt1cPhaX9vpiC37uBgknOj8XmmJF-tm58LMyc_LQ1j8fCjH1hJj8lH118w84Gs4_09mlesO-fb75dfynvv97eXa_vSytrkUpTgxKi46qRthYEbdcLtKIZqAbbkBXQttIgN6azXe5iDQ2I_cZwzGgrxAX7cLrrY3I6WpfIbq0fR7JJc97ITnGVqY8nKvf4OVNM-uDiUsyM5OeoUTVtLbGVmFFxQm3wMQYa9BTcwYSjRtCLab3Tf03rxbQGrrPpvPX-KWDeHKj_v_NPbQY-nQDKMn45CsuvNFrqXVhe7b17NuAPEpuOcQ</recordid><startdate>20170301</startdate><enddate>20170301</enddate><creator>Shen, Xue</creator><creator>Kan, Shifeng</creator><creator>Liu, Zhen</creator><creator>Lu, Guang</creator><creator>Zhang, Xiaoyan</creator><creator>Chen, Yingyu</creator><creator>Bai, Yun</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>OTOTI</scope></search><sort><creationdate>20170301</creationdate><title>EVA1A inhibits GBM cell proliferation by inducing autophagy and apoptosis</title><author>Shen, Xue ; Kan, Shifeng ; Liu, Zhen ; Lu, Guang ; Zhang, Xiaoyan ; Chen, Yingyu ; Bai, Yun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c453t-a5083392864c53e079d31c36fe50c6ec30774a12aa9c9090caef11dba2179d733</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>ADENOVIRUS</topic><topic>Animals</topic><topic>Anti-tumor activity</topic><topic>APOPTOSIS</topic><topic>Autophagy</topic><topic>Blotting, Western</topic><topic>BUDR</topic><topic>Cell Adhesion Molecules - genetics</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>CELL PROLIFERATION</topic><topic>DOSES</topic><topic>ENDOPLASMIC RETICULUM</topic><topic>EVA1A</topic><topic>Female</topic><topic>GBM</topic><topic>Glioblastoma - genetics</topic><topic>Glioblastoma - metabolism</topic><topic>Glioblastoma - pathology</topic><topic>GLIOMAS</topic><topic>Humans</topic><topic>IN VITRO</topic><topic>IN VIVO</topic><topic>INACTIVATION</topic><topic>INDUCTION</topic><topic>INHIBITION</topic><topic>LYSOSOMES</topic><topic>MICE</topic><topic>Mice, Inbred NOD</topic><topic>Mice, SCID</topic><topic>mTOR/RPS6KB1</topic><topic>PHOSPHOTRANSFERASES</topic><topic>PLANT GROWTH</topic><topic>POLYPEPTIDES</topic><topic>Proliferation</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>REGULATIONS</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>TIME DEPENDENCE</topic><topic>TUMOR CELLS</topic><topic>Tumor Cells, Cultured</topic><topic>VECTORS</topic><topic>VISIBLE RADIATION</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shen, Xue</creatorcontrib><creatorcontrib>Kan, Shifeng</creatorcontrib><creatorcontrib>Liu, Zhen</creatorcontrib><creatorcontrib>Lu, Guang</creatorcontrib><creatorcontrib>Zhang, Xiaoyan</creatorcontrib><creatorcontrib>Chen, Yingyu</creatorcontrib><creatorcontrib>Bai, Yun</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>OSTI.GOV</collection><jtitle>Experimental cell research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shen, Xue</au><au>Kan, Shifeng</au><au>Liu, Zhen</au><au>Lu, Guang</au><au>Zhang, Xiaoyan</au><au>Chen, Yingyu</au><au>Bai, Yun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>EVA1A inhibits GBM cell proliferation by inducing autophagy and apoptosis</atitle><jtitle>Experimental cell research</jtitle><addtitle>Exp Cell Res</addtitle><date>2017-03-01</date><risdate>2017</risdate><volume>352</volume><issue>1</issue><spage>130</spage><epage>138</epage><pages>130-138</pages><issn>0014-4827</issn><eissn>1090-2422</eissn><abstract>Eva-1 homolog A (EVA1A) is a novel lysosome and endoplasmic reticulum-associated protein involved in autophagy and apoptosis. In this study, we constructed a recombinant adenovirus 5-EVA1A vector (Ad5-EVA1A) to overexpress EVA1A in glioblastoma (GBM) cell lines and evaluated its anti-tumor activities in vitro and in vivo. We found that overexpression of EVA1A in three GBM cell lines (U251, U87 and SHG44) resulted in a suppression of tumor cell growth via activation of autophagy and induction of cell apoptosis in a dose- and time-dependent manner. EVA1A-mediated autophagy was associated with inactivation of the mTOR/RPS6KB1 signaling pathway. Furthermore in vivo, overexpression of EVA1A successfully inhibited tumor growth in NOD/SCID mice. Our data suggest that EVA1A-induced autophagy and apoptosis play a role in suppressing the development of GBM and their up-regulation may be an effective method for treating this form of cancer.
•Overexpression of EVA1A suppresses GBM cell growth.•EVA1A induces autophagy through the mTOR/RPS6KB1 pathway.•EVA1A induces GBM cell apoptosis.•EVA1A inhibits the development of GBM in vivo.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>28185834</pmid><doi>10.1016/j.yexcr.2017.02.003</doi><tpages>9</tpages></addata></record> |
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| ispartof | Experimental cell research, 2017-03, Vol.352 (1), p.130-138 |
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| subjects | 60 APPLIED LIFE SCIENCES ADENOVIRUS Animals Anti-tumor activity APOPTOSIS Autophagy Blotting, Western BUDR Cell Adhesion Molecules - genetics Cell Adhesion Molecules - metabolism CELL PROLIFERATION DOSES ENDOPLASMIC RETICULUM EVA1A Female GBM Glioblastoma - genetics Glioblastoma - metabolism Glioblastoma - pathology GLIOMAS Humans IN VITRO IN VIVO INACTIVATION INDUCTION INHIBITION LYSOSOMES MICE Mice, Inbred NOD Mice, SCID mTOR/RPS6KB1 PHOSPHOTRANSFERASES PLANT GROWTH POLYPEPTIDES Proliferation Real-Time Polymerase Chain Reaction REGULATIONS Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics TIME DEPENDENCE TUMOR CELLS Tumor Cells, Cultured VECTORS VISIBLE RADIATION Xenograft Model Antitumor Assays |
| title | EVA1A inhibits GBM cell proliferation by inducing autophagy and apoptosis |
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