Inhibition of mTOR pathway attenuates migration and invasion of gallbladder cancer via EMT inhibition
Gallbladder cancer (GBC) is an aggressive disease in which epithelial-mesenchymal transition (EMT) plays a critical role. Whether inhibition of mTOR effects via EMT reversal in GBC remains unclear. Using genetic and pharmacologic inhibitions of mTOR, we investigated the changes of EMT levels in GBC...
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| Veröffentlicht in: | Molecular biology reports 2014-07, Vol.41 (7), p.4507-4512 |
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| creator | Zong, Huajie Yin, Baobing Zhou, Huading Cai, Duan Ma, Baojin Xiang, Yang |
| description | Gallbladder cancer (GBC) is an aggressive disease in which epithelial-mesenchymal transition (EMT) plays a critical role. Whether inhibition of mTOR effects via EMT reversal in GBC remains unclear. Using genetic and pharmacologic inhibitions of mTOR, we investigated the changes of EMT levels in GBC cells. Expressions of EMT related genes were also studied. Migration and invasion assays were carried out and in vivo tumour metastasis mouse models were established. Circulating tumour DNA was quantified. We used EMT index (ratio of Vimentin/Ecadherin expression) to profile EMT levels. We found that inhibition of mTOR using shRNAs and rapamycin inhibited EMT in GBC-SD gallbladder cancer cells. Inhibition of mTOR inhibited EMT in GBC-SD cells in TGF-β-dependent manner, which was contributed majorly by mTORC2 inhibition. Rapamycin decreased invasiveness and migration of GBC-SD cells in vitro and in vivo. We have in the current study shown that rapamycin diminishes the ability of invasion and migration of GBC via inhibition of TGF-β-dependent EMT. Our findings contribute to the understanding of the carcinogenesis of GBC. |
| doi_str_mv | 10.1007/s11033-014-3321-4 |
| format | Article |
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Whether inhibition of mTOR effects via EMT reversal in GBC remains unclear. Using genetic and pharmacologic inhibitions of mTOR, we investigated the changes of EMT levels in GBC cells. Expressions of EMT related genes were also studied. Migration and invasion assays were carried out and in vivo tumour metastasis mouse models were established. Circulating tumour DNA was quantified. We used EMT index (ratio of Vimentin/Ecadherin expression) to profile EMT levels. We found that inhibition of mTOR using shRNAs and rapamycin inhibited EMT in GBC-SD gallbladder cancer cells. Inhibition of mTOR inhibited EMT in GBC-SD cells in TGF-β-dependent manner, which was contributed majorly by mTORC2 inhibition. Rapamycin decreased invasiveness and migration of GBC-SD cells in vitro and in vivo. We have in the current study shown that rapamycin diminishes the ability of invasion and migration of GBC via inhibition of TGF-β-dependent EMT. Our findings contribute to the understanding of the carcinogenesis of GBC.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-014-3321-4</identifier><identifier>PMID: 24623408</identifier><language>eng</language><publisher>Dordrecht: Springer-Verlag</publisher><subject>Animal Anatomy ; Animal Biochemistry ; animal models ; Animals ; Biomedical and Life Sciences ; Cadherins - genetics ; Cadherins - metabolism ; Cancer ; carcinogenesis ; Cell Line, Tumor ; Cell Movement - drug effects ; DNA ; Epithelial-Mesenchymal Transition - drug effects ; Epithelial-Mesenchymal Transition - genetics ; gall bladder ; Gallbladder ; Gallbladder Neoplasms - drug therapy ; Gallbladder Neoplasms - genetics ; Gallbladder Neoplasms - metabolism ; Gallbladder Neoplasms - pathology ; Gene Expression Regulation, Neoplastic ; genes ; Histology ; Humans ; Immunosuppressive Agents - pharmacology ; Life Sciences ; Male ; Mechanistic Target of Rapamycin Complex 2 ; metastasis ; Mice ; Mice, Nude ; Molecular biology ; Morphology ; Multiprotein Complexes - antagonists & inhibitors ; Multiprotein Complexes - genetics ; Multiprotein Complexes - metabolism ; Neoplasm Invasiveness ; neoplasms ; Pathogenesis ; rapamycin ; RNA, Small Interfering - genetics ; RNA, Small Interfering - metabolism ; Signal Transduction - drug effects ; Sirolimus - pharmacology ; TOR Serine-Threonine Kinases - antagonists & inhibitors ; TOR Serine-Threonine Kinases - genetics ; TOR Serine-Threonine Kinases - metabolism ; Transforming Growth Factor beta - genetics ; Transforming Growth Factor beta - metabolism ; vimentin ; Vimentin - genetics ; Vimentin - metabolism</subject><ispartof>Molecular biology reports, 2014-07, Vol.41 (7), p.4507-4512</ispartof><rights>Springer Science+Business Media Dordrecht 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-8929227547b79523e307923d70092bf5513b25b64a41883adeda4ca19ba754d53</citedby><cites>FETCH-LOGICAL-c565t-8929227547b79523e307923d70092bf5513b25b64a41883adeda4ca19ba754d53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11033-014-3321-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-014-3321-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24623408$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zong, Huajie</creatorcontrib><creatorcontrib>Yin, Baobing</creatorcontrib><creatorcontrib>Zhou, Huading</creatorcontrib><creatorcontrib>Cai, Duan</creatorcontrib><creatorcontrib>Ma, Baojin</creatorcontrib><creatorcontrib>Xiang, Yang</creatorcontrib><title>Inhibition of mTOR pathway attenuates migration and invasion of gallbladder cancer via EMT inhibition</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>Gallbladder cancer (GBC) is an aggressive disease in which epithelial-mesenchymal transition (EMT) plays a critical role. Whether inhibition of mTOR effects via EMT reversal in GBC remains unclear. Using genetic and pharmacologic inhibitions of mTOR, we investigated the changes of EMT levels in GBC cells. Expressions of EMT related genes were also studied. Migration and invasion assays were carried out and in vivo tumour metastasis mouse models were established. Circulating tumour DNA was quantified. We used EMT index (ratio of Vimentin/Ecadherin expression) to profile EMT levels. We found that inhibition of mTOR using shRNAs and rapamycin inhibited EMT in GBC-SD gallbladder cancer cells. Inhibition of mTOR inhibited EMT in GBC-SD cells in TGF-β-dependent manner, which was contributed majorly by mTORC2 inhibition. Rapamycin decreased invasiveness and migration of GBC-SD cells in vitro and in vivo. We have in the current study shown that rapamycin diminishes the ability of invasion and migration of GBC via inhibition of TGF-β-dependent EMT. Our findings contribute to the understanding of the carcinogenesis of GBC.</description><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>animal models</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Cadherins - genetics</subject><subject>Cadherins - metabolism</subject><subject>Cancer</subject><subject>carcinogenesis</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>DNA</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>gall bladder</subject><subject>Gallbladder</subject><subject>Gallbladder Neoplasms - drug therapy</subject><subject>Gallbladder Neoplasms - genetics</subject><subject>Gallbladder Neoplasms - metabolism</subject><subject>Gallbladder Neoplasms - pathology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>genes</subject><subject>Histology</subject><subject>Humans</subject><subject>Immunosuppressive Agents - 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genetics</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>vimentin</subject><subject>Vimentin - genetics</subject><subject>Vimentin - metabolism</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kUFv1DAQhS0EokvhB3CBSFy4BMYeO46PqCq0UlEl2J6tSeJsXSXOYiet-u_rki1CHDiNNPO9N6N5jL3l8IkD6M-Jc0AsgcsSUfBSPmMbrjSW0uj6OdsAQm7Wih-xVyndAIDkWr1kR0JWAiXUG-bOw7Vv_OynUEx9MW4vfxR7mq_v6L6geXZhodmlYvS7SL8hCl3hwy2lg2JHw9AM1HUuFi2FNpdbT8Xp923Gnqxfsxc9Dcm9OdRjdvX1dHtyVl5cfjs_-XJRtqpSc1kbYYTQSupGGyXQIWgjsNMARjS9UhwboZpKkuR1jdS5jmRL3DSURZ3CY_Zx9d3H6dfi0mxHn1o3DBTctCSLXGGN-Tkmox_-QW-mJYZ8nc1Q3gqoq0zxlWrjlFJ0vd1HP1K8txzsYwZ2zcDmDOxjBlZmzbuD89KMrvujeHp6BsQKpDwKOxf_Wv0f1_erqKfJ0i76ZK9-igwAcKxNhfgAg9eY8Q</recordid><startdate>20140701</startdate><enddate>20140701</enddate><creator>Zong, Huajie</creator><creator>Yin, Baobing</creator><creator>Zhou, Huading</creator><creator>Cai, Duan</creator><creator>Ma, Baojin</creator><creator>Xiang, Yang</creator><general>Springer-Verlag</general><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>FBQ</scope><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>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7S9</scope><scope>L.6</scope></search><sort><creationdate>20140701</creationdate><title>Inhibition of mTOR pathway attenuates migration and invasion of gallbladder cancer via EMT inhibition</title><author>Zong, Huajie ; Yin, Baobing ; Zhou, Huading ; Cai, Duan ; Ma, Baojin ; Xiang, Yang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c565t-8929227547b79523e307923d70092bf5513b25b64a41883adeda4ca19ba754d53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>animal models</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Cadherins - 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Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zong, Huajie</au><au>Yin, Baobing</au><au>Zhou, Huading</au><au>Cai, Duan</au><au>Ma, Baojin</au><au>Xiang, Yang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of mTOR pathway attenuates migration and invasion of gallbladder cancer via EMT inhibition</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2014-07-01</date><risdate>2014</risdate><volume>41</volume><issue>7</issue><spage>4507</spage><epage>4512</epage><pages>4507-4512</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Gallbladder cancer (GBC) is an aggressive disease in which epithelial-mesenchymal transition (EMT) plays a critical role. Whether inhibition of mTOR effects via EMT reversal in GBC remains unclear. Using genetic and pharmacologic inhibitions of mTOR, we investigated the changes of EMT levels in GBC cells. Expressions of EMT related genes were also studied. Migration and invasion assays were carried out and in vivo tumour metastasis mouse models were established. Circulating tumour DNA was quantified. We used EMT index (ratio of Vimentin/Ecadherin expression) to profile EMT levels. We found that inhibition of mTOR using shRNAs and rapamycin inhibited EMT in GBC-SD gallbladder cancer cells. Inhibition of mTOR inhibited EMT in GBC-SD cells in TGF-β-dependent manner, which was contributed majorly by mTORC2 inhibition. Rapamycin decreased invasiveness and migration of GBC-SD cells in vitro and in vivo. We have in the current study shown that rapamycin diminishes the ability of invasion and migration of GBC via inhibition of TGF-β-dependent EMT. Our findings contribute to the understanding of the carcinogenesis of GBC.</abstract><cop>Dordrecht</cop><pub>Springer-Verlag</pub><pmid>24623408</pmid><doi>10.1007/s11033-014-3321-4</doi><tpages>6</tpages></addata></record> |
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| subjects | Animal Anatomy Animal Biochemistry animal models Animals Biomedical and Life Sciences Cadherins - genetics Cadherins - metabolism Cancer carcinogenesis Cell Line, Tumor Cell Movement - drug effects DNA Epithelial-Mesenchymal Transition - drug effects Epithelial-Mesenchymal Transition - genetics gall bladder Gallbladder Gallbladder Neoplasms - drug therapy Gallbladder Neoplasms - genetics Gallbladder Neoplasms - metabolism Gallbladder Neoplasms - pathology Gene Expression Regulation, Neoplastic genes Histology Humans Immunosuppressive Agents - pharmacology Life Sciences Male Mechanistic Target of Rapamycin Complex 2 metastasis Mice Mice, Nude Molecular biology Morphology Multiprotein Complexes - antagonists & inhibitors Multiprotein Complexes - genetics Multiprotein Complexes - metabolism Neoplasm Invasiveness neoplasms Pathogenesis rapamycin RNA, Small Interfering - genetics RNA, Small Interfering - metabolism Signal Transduction - drug effects Sirolimus - pharmacology TOR Serine-Threonine Kinases - antagonists & inhibitors TOR Serine-Threonine Kinases - genetics TOR Serine-Threonine Kinases - metabolism Transforming Growth Factor beta - genetics Transforming Growth Factor beta - metabolism vimentin Vimentin - genetics Vimentin - metabolism |
| title | Inhibition of mTOR pathway attenuates migration and invasion of gallbladder cancer via EMT inhibition |
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