Under hypoxia conditions contactin-1 regulates the migration of Mkn45 cells through the RhoA pathway
Recent studies have suggested that contactin-1 has a key role in cancer cell proliferation and migration, however the detailed mechanism of this process is still unclear. Here, human gastric cancer cell line MKN45 was employed. It was found that under hypoxia conditions contactin-1 mRNA and protein...
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| Veröffentlicht in: | Molecular biology (New York) 2015, Vol.49 (1), p.112-119 |
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| creator | Yang, G. Song, J. -G. Li, Y. Gong, S. -P. |
| description | Recent studies have suggested that contactin-1 has a key role in cancer cell proliferation and migration, however the detailed mechanism of this process is still unclear. Here, human gastric cancer cell line MKN45 was employed. It was found that under hypoxia conditions contactin-1 mRNA and protein levels were both up-regulated by HIF-1α expression. Furthermore, although hypoxia increased the migration rate of MKN45 cells,
contactin-1
(
CNTN1
) shRNA reversed this process. Meanwhile,
RhoA V14
and
RhoA V14 N19
mutation constructs were employed, and it was found that constitutively active form of
RhoA
reversed the cell migration suppression induced by contactin-1 knockdown, while dominant-negative form of
RhoA
blocked hypoxia induced hypermigration. Apart from this, contactin-1 displayed the ability to phosphorylate the RhoA activator p115 RhoGEF. Thus, under hypoxia conditions, elevated HIF-1α seems to up-regulate contactin-1 expression and by this activate RhoA and facilitate migration of cancer cells. |
| doi_str_mv | 10.1134/S0026893315010185 |
| format | Article |
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contactin-1
(
CNTN1
) shRNA reversed this process. Meanwhile,
RhoA V14
and
RhoA V14 N19
mutation constructs were employed, and it was found that constitutively active form of
RhoA
reversed the cell migration suppression induced by contactin-1 knockdown, while dominant-negative form of
RhoA
blocked hypoxia induced hypermigration. Apart from this, contactin-1 displayed the ability to phosphorylate the RhoA activator p115 RhoGEF. Thus, under hypoxia conditions, elevated HIF-1α seems to up-regulate contactin-1 expression and by this activate RhoA and facilitate migration of cancer cells.</description><identifier>ISSN: 0026-8933</identifier><identifier>EISSN: 1608-3245</identifier><identifier>DOI: 10.1134/S0026893315010185</identifier><language>eng</language><publisher>Moscow: Pleiades Publishing</publisher><subject>Biochemistry ; Biomedical and Life Sciences ; Cell Molecular Biology ; Cellular biology ; Gastric cancer ; Human Genetics ; Hypoxia ; Life Sciences ; MicroRNAs ; Molecular biology ; Proteins</subject><ispartof>Molecular biology (New York), 2015, Vol.49 (1), p.112-119</ispartof><rights>Pleiades Publishing, Inc. 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c316t-e489ee221e99a9493db9de3d4ba81ee467c88f2492bce02fabe5d8d4d0cc56263</citedby><cites>FETCH-LOGICAL-c316t-e489ee221e99a9493db9de3d4ba81ee467c88f2492bce02fabe5d8d4d0cc56263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1134/S0026893315010185$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1134/S0026893315010185$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids></links><search><creatorcontrib>Yang, G.</creatorcontrib><creatorcontrib>Song, J. -G.</creatorcontrib><creatorcontrib>Li, Y.</creatorcontrib><creatorcontrib>Gong, S. -P.</creatorcontrib><title>Under hypoxia conditions contactin-1 regulates the migration of Mkn45 cells through the RhoA pathway</title><title>Molecular biology (New York)</title><addtitle>Mol Biol</addtitle><description>Recent studies have suggested that contactin-1 has a key role in cancer cell proliferation and migration, however the detailed mechanism of this process is still unclear. Here, human gastric cancer cell line MKN45 was employed. It was found that under hypoxia conditions contactin-1 mRNA and protein levels were both up-regulated by HIF-1α expression. Furthermore, although hypoxia increased the migration rate of MKN45 cells,
contactin-1
(
CNTN1
) shRNA reversed this process. Meanwhile,
RhoA V14
and
RhoA V14 N19
mutation constructs were employed, and it was found that constitutively active form of
RhoA
reversed the cell migration suppression induced by contactin-1 knockdown, while dominant-negative form of
RhoA
blocked hypoxia induced hypermigration. Apart from this, contactin-1 displayed the ability to phosphorylate the RhoA activator p115 RhoGEF. Thus, under hypoxia conditions, elevated HIF-1α seems to up-regulate contactin-1 expression and by this activate RhoA and facilitate migration of cancer cells.</description><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Molecular Biology</subject><subject>Cellular biology</subject><subject>Gastric cancer</subject><subject>Human Genetics</subject><subject>Hypoxia</subject><subject>Life Sciences</subject><subject>MicroRNAs</subject><subject>Molecular biology</subject><subject>Proteins</subject><issn>0026-8933</issn><issn>1608-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kMtKxDAUhoMoOI4-gLuA62quNV0OgzcYEdRZlzQ5vYydpiYpOm9v67gQxNU58H_fOfAjdE7JJaVcXL0QwlKVcU4loYQqeYBmNCUq4UzIQzSb4mTKj9FJCBsyQoSyGbLrzoLH9a53n43GxnW2iY3rwrRGbWLTJRR7qIZWRwg41oC3TeX1BGFX4se3TkhsoG2n0Luhqr-h59otcK9j_aF3p-io1G2As585R-vbm9flfbJ6untYLlaJ4TSNCQiVATBGIct0JjJui8wCt6LQigKI9NooVTKRscIAYaUuQFplhSXGyJSlfI4u9nd7794HCDHfuMF348ucplISNbkjRfeU8S4ED2Xe-2ar_S6nJJ_KzP-UOTps74SR7Srwvy7_K30BgfF2zg</recordid><startdate>2015</startdate><enddate>2015</enddate><creator>Yang, G.</creator><creator>Song, J. -G.</creator><creator>Li, Y.</creator><creator>Gong, S. -P.</creator><general>Pleiades Publishing</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</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>H94</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></search><sort><creationdate>2015</creationdate><title>Under hypoxia conditions contactin-1 regulates the migration of Mkn45 cells through the RhoA pathway</title><author>Yang, G. ; Song, J. -G. ; Li, Y. ; Gong, S. -P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c316t-e489ee221e99a9493db9de3d4ba81ee467c88f2492bce02fabe5d8d4d0cc56263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cell Molecular Biology</topic><topic>Cellular biology</topic><topic>Gastric cancer</topic><topic>Human Genetics</topic><topic>Hypoxia</topic><topic>Life Sciences</topic><topic>MicroRNAs</topic><topic>Molecular biology</topic><topic>Proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, G.</creatorcontrib><creatorcontrib>Song, J. -G.</creatorcontrib><creatorcontrib>Li, Y.</creatorcontrib><creatorcontrib>Gong, S. -P.</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Molecular biology (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, G.</au><au>Song, J. -G.</au><au>Li, Y.</au><au>Gong, S. -P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Under hypoxia conditions contactin-1 regulates the migration of Mkn45 cells through the RhoA pathway</atitle><jtitle>Molecular biology (New York)</jtitle><stitle>Mol Biol</stitle><date>2015</date><risdate>2015</risdate><volume>49</volume><issue>1</issue><spage>112</spage><epage>119</epage><pages>112-119</pages><issn>0026-8933</issn><eissn>1608-3245</eissn><abstract>Recent studies have suggested that contactin-1 has a key role in cancer cell proliferation and migration, however the detailed mechanism of this process is still unclear. Here, human gastric cancer cell line MKN45 was employed. It was found that under hypoxia conditions contactin-1 mRNA and protein levels were both up-regulated by HIF-1α expression. Furthermore, although hypoxia increased the migration rate of MKN45 cells,
contactin-1
(
CNTN1
) shRNA reversed this process. Meanwhile,
RhoA V14
and
RhoA V14 N19
mutation constructs were employed, and it was found that constitutively active form of
RhoA
reversed the cell migration suppression induced by contactin-1 knockdown, while dominant-negative form of
RhoA
blocked hypoxia induced hypermigration. Apart from this, contactin-1 displayed the ability to phosphorylate the RhoA activator p115 RhoGEF. Thus, under hypoxia conditions, elevated HIF-1α seems to up-regulate contactin-1 expression and by this activate RhoA and facilitate migration of cancer cells.</abstract><cop>Moscow</cop><pub>Pleiades Publishing</pub><doi>10.1134/S0026893315010185</doi><tpages>8</tpages></addata></record> |
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| subjects | Biochemistry Biomedical and Life Sciences Cell Molecular Biology Cellular biology Gastric cancer Human Genetics Hypoxia Life Sciences MicroRNAs Molecular biology Proteins |
| title | Under hypoxia conditions contactin-1 regulates the migration of Mkn45 cells through the RhoA pathway |
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