Functions of the AP-2α gene in activating apoptosis and inhibiting proliferation of gastric cancer cells both in vitro and in vivo
This study was designed to investigate the potential function of the activating protein 2α (AP-2α) gene in controlling the proliferation and apoptosis of gastric cancer. Gastric cancer cell line MCG-803 cells and normal cell line GES-1 cells were selected to transfect pcDNA3.1(+)-AP-2α and pcDNA3.1(...
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| Veröffentlicht in: | Archives of medical science 2017-10, Vol.13 (6), p.1255-1261 |
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| container_title | Archives of medical science |
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| creator | Zeng, Changqing Liu, Zhimin Zhang, Jian Fang, Hongwei Fang, Cheng Wang, Yueming Seeruttun, Sharvesh Raj Chen, Jun Huang, Liangxiang Wang, Wei |
| description | This study was designed to investigate the potential function of the activating protein 2α (AP-2α) gene in controlling the proliferation and apoptosis of gastric cancer.
Gastric cancer cell line MCG-803 cells and normal cell line GES-1 cells were selected to transfect pcDNA3.1(+)-AP-2α and pcDNA3.1(+) plasmids, respectively. Both mRNA and protein levels of AP-2α in each group transfected with the pcDNA3.1(+)-AP-2α plasmids were up-regulated after 48 h by real-time PCR and Western blotting analysis, leading to marked proliferation inhibition and significant cell cycle arrest.
pcDNA3.1(+)-AP-2α reduced tumor tissue growth in a subcutaneous tumor gastric carcinoma nude mouse model. Protein over-expression of AP-2α in the nude mouse model was accompanied by down-regulation of Blc-2 and ErbB2, resulting in the up-regulation of caspase-3, -8, and -9, ERα and p21
.
The reintroduction of the AP-2α gene by pcDNA3.1 could inhibit gastric tumor growth
and
, which may be an alternative future therapeutic molecular target for human gastric cancer. |
| doi_str_mv | 10.5114/aoms.2017.71064 |
| format | Article |
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Gastric cancer cell line MCG-803 cells and normal cell line GES-1 cells were selected to transfect pcDNA3.1(+)-AP-2α and pcDNA3.1(+) plasmids, respectively. Both mRNA and protein levels of AP-2α in each group transfected with the pcDNA3.1(+)-AP-2α plasmids were up-regulated after 48 h by real-time PCR and Western blotting analysis, leading to marked proliferation inhibition and significant cell cycle arrest.
pcDNA3.1(+)-AP-2α reduced tumor tissue growth in a subcutaneous tumor gastric carcinoma nude mouse model. Protein over-expression of AP-2α in the nude mouse model was accompanied by down-regulation of Blc-2 and ErbB2, resulting in the up-regulation of caspase-3, -8, and -9, ERα and p21
.
The reintroduction of the AP-2α gene by pcDNA3.1 could inhibit gastric tumor growth
and
, which may be an alternative future therapeutic molecular target for human gastric cancer.</description><identifier>ISSN: 1734-1922</identifier><identifier>EISSN: 1896-9151</identifier><identifier>DOI: 10.5114/aoms.2017.71064</identifier><identifier>PMID: 29181055</identifier><language>eng</language><publisher>Poland: Termedia Publishing House</publisher><subject>Apoptosis ; Basic Research ; Cell cycle ; Gastric cancer ; Plasmids ; Proteins</subject><ispartof>Archives of medical science, 2017-10, Vol.13 (6), p.1255-1261</ispartof><rights>Copyright Termedia Publishing House 2017</rights><rights>Copyright: © 2017 Termedia & Banach 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-8431cae3c4506e75463dbf431d152c0922888efa305fb8d780e86ad29e4c13a53</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5701697/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5701697/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29181055$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zeng, Changqing</creatorcontrib><creatorcontrib>Liu, Zhimin</creatorcontrib><creatorcontrib>Zhang, Jian</creatorcontrib><creatorcontrib>Fang, Hongwei</creatorcontrib><creatorcontrib>Fang, Cheng</creatorcontrib><creatorcontrib>Wang, Yueming</creatorcontrib><creatorcontrib>Seeruttun, Sharvesh Raj</creatorcontrib><creatorcontrib>Chen, Jun</creatorcontrib><creatorcontrib>Huang, Liangxiang</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><title>Functions of the AP-2α gene in activating apoptosis and inhibiting proliferation of gastric cancer cells both in vitro and in vivo</title><title>Archives of medical science</title><addtitle>Arch Med Sci</addtitle><description>This study was designed to investigate the potential function of the activating protein 2α (AP-2α) gene in controlling the proliferation and apoptosis of gastric cancer.
Gastric cancer cell line MCG-803 cells and normal cell line GES-1 cells were selected to transfect pcDNA3.1(+)-AP-2α and pcDNA3.1(+) plasmids, respectively. Both mRNA and protein levels of AP-2α in each group transfected with the pcDNA3.1(+)-AP-2α plasmids were up-regulated after 48 h by real-time PCR and Western blotting analysis, leading to marked proliferation inhibition and significant cell cycle arrest.
pcDNA3.1(+)-AP-2α reduced tumor tissue growth in a subcutaneous tumor gastric carcinoma nude mouse model. Protein over-expression of AP-2α in the nude mouse model was accompanied by down-regulation of Blc-2 and ErbB2, resulting in the up-regulation of caspase-3, -8, and -9, ERα and p21
.
The reintroduction of the AP-2α gene by pcDNA3.1 could inhibit gastric tumor growth
and
, which may be an alternative future therapeutic molecular target for human gastric cancer.</description><subject>Apoptosis</subject><subject>Basic Research</subject><subject>Cell cycle</subject><subject>Gastric cancer</subject><subject>Plasmids</subject><subject>Proteins</subject><issn>1734-1922</issn><issn>1896-9151</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNpdkc9uFSEYxYnR2FpduzMkbrqZWz7-zAwbk6axatJEF7omDMPcSzMXRmBu4ton8kX6TEJ7bdQV8J3DD04OQq-BbAQAv9BhnzaUQLfpgLT8CTqFXraNBAFPy75jvAFJ6Ql6kdItIbxM4Dk6oRJ6IEKcop_XqzfZBZ9wmHDeWXz5paF3v_DWeoudx7qoB52d32K9hCWH5BLWfizazg3uXlhimN1ko66gytnqlKMz2GhvbMTGznPCQ8i7Sjy4HMMRUQ6H8BI9m_Sc7Kvjeoa-Xb__evWxufn84dPV5U1jOIXc9JyB0ZYZLkhrO8FbNg5TGY4gqCElZt_3dtKMiGnox64ntm_1SKXlBpgW7Ay9e-Au67C3o7E-Rz2rJbq9jj9U0E79q3i3U9twUKIj0MquAM6PgBi-rzZltXephtPehjUpkK2UlDBR33r7n_U2rNGXeNVFy--B0uK6eHCZGFKKdnr8DBBVC1a1YFULVvcFlxtv_s7w6P_TKPsNgeikOg</recordid><startdate>20171001</startdate><enddate>20171001</enddate><creator>Zeng, Changqing</creator><creator>Liu, Zhimin</creator><creator>Zhang, Jian</creator><creator>Fang, Hongwei</creator><creator>Fang, Cheng</creator><creator>Wang, Yueming</creator><creator>Seeruttun, Sharvesh Raj</creator><creator>Chen, Jun</creator><creator>Huang, Liangxiang</creator><creator>Wang, Wei</creator><general>Termedia Publishing House</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BYOGL</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20171001</creationdate><title>Functions of the AP-2α gene in activating apoptosis and inhibiting proliferation of gastric cancer cells both in vitro and in vivo</title><author>Zeng, Changqing ; Liu, Zhimin ; Zhang, Jian ; Fang, Hongwei ; Fang, Cheng ; Wang, Yueming ; Seeruttun, Sharvesh Raj ; Chen, Jun ; Huang, Liangxiang ; Wang, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-8431cae3c4506e75463dbf431d152c0922888efa305fb8d780e86ad29e4c13a53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Apoptosis</topic><topic>Basic Research</topic><topic>Cell cycle</topic><topic>Gastric cancer</topic><topic>Plasmids</topic><topic>Proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zeng, Changqing</creatorcontrib><creatorcontrib>Liu, Zhimin</creatorcontrib><creatorcontrib>Zhang, Jian</creatorcontrib><creatorcontrib>Fang, Hongwei</creatorcontrib><creatorcontrib>Fang, Cheng</creatorcontrib><creatorcontrib>Wang, Yueming</creatorcontrib><creatorcontrib>Seeruttun, Sharvesh Raj</creatorcontrib><creatorcontrib>Chen, Jun</creatorcontrib><creatorcontrib>Huang, Liangxiang</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>East Europe, Central Europe Database</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>Publicly Available Content Database</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>Archives of medical science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zeng, Changqing</au><au>Liu, Zhimin</au><au>Zhang, Jian</au><au>Fang, Hongwei</au><au>Fang, Cheng</au><au>Wang, Yueming</au><au>Seeruttun, Sharvesh Raj</au><au>Chen, Jun</au><au>Huang, Liangxiang</au><au>Wang, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Functions of the AP-2α gene in activating apoptosis and inhibiting proliferation of gastric cancer cells both in vitro and in vivo</atitle><jtitle>Archives of medical science</jtitle><addtitle>Arch Med Sci</addtitle><date>2017-10-01</date><risdate>2017</risdate><volume>13</volume><issue>6</issue><spage>1255</spage><epage>1261</epage><pages>1255-1261</pages><issn>1734-1922</issn><eissn>1896-9151</eissn><abstract>This study was designed to investigate the potential function of the activating protein 2α (AP-2α) gene in controlling the proliferation and apoptosis of gastric cancer.
Gastric cancer cell line MCG-803 cells and normal cell line GES-1 cells were selected to transfect pcDNA3.1(+)-AP-2α and pcDNA3.1(+) plasmids, respectively. Both mRNA and protein levels of AP-2α in each group transfected with the pcDNA3.1(+)-AP-2α plasmids were up-regulated after 48 h by real-time PCR and Western blotting analysis, leading to marked proliferation inhibition and significant cell cycle arrest.
pcDNA3.1(+)-AP-2α reduced tumor tissue growth in a subcutaneous tumor gastric carcinoma nude mouse model. Protein over-expression of AP-2α in the nude mouse model was accompanied by down-regulation of Blc-2 and ErbB2, resulting in the up-regulation of caspase-3, -8, and -9, ERα and p21
.
The reintroduction of the AP-2α gene by pcDNA3.1 could inhibit gastric tumor growth
and
, which may be an alternative future therapeutic molecular target for human gastric cancer.</abstract><cop>Poland</cop><pub>Termedia Publishing House</pub><pmid>29181055</pmid><doi>10.5114/aoms.2017.71064</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
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| source | DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; PubMed Central |
| subjects | Apoptosis Basic Research Cell cycle Gastric cancer Plasmids Proteins |
| title | Functions of the AP-2α gene in activating apoptosis and inhibiting proliferation of gastric cancer cells both in vitro and in vivo |
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