TRPV4 promotes the migration and invasion of glioma cells via AKT/Rac1 signaling
Experimental evidence indicates a critical role of TRPV4 (Transient Receptor Potential Vanilloid 4) in controlling the cell migratory activity of multiple tumors. However, the oncogenic role of TRPV4 in glioma still remains elusive. In this study, we tried to investigate the oncogenic role of TRPV4...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2018-09, Vol.503 (2), p.876-881 |
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| creator | Ou-yang, Qing Li, Bing Xu, Minhui Liang, Hong |
| description | Experimental evidence indicates a critical role of TRPV4 (Transient Receptor Potential Vanilloid 4) in controlling the cell migratory activity of multiple tumors. However, the oncogenic role of TRPV4 in glioma still remains elusive. In this study, we tried to investigate the oncogenic role of TRPV4 in glioma. We found that the expression levels of TRPV4 were upregulated in glioma and the high levels of TRPV4 indicated a worse prognosis in patients with glioma. TRPV4 was critical for glioma migration and invasion: activating TRPV4 by agonist GSK1016790 A enhanced glioma migration and invasion, while, the specific TRPV4 antagonist HC-067047 suppressed glioma migration and invasion. Mechanically, activated TRPV4 promoted the activation of Rac1 (Ras-related C3 botulinum toxin substrate 1) by targeting the AKT for phosphorylation, then enhanced glioma migration and invasion. All these results suggested that TRPV4 accelerates glioma migration and invasion through the AKT/Rac1 signaling, and TRPV4 might be considered as a potential target for glioma therapy.
•TRPV4 is upregulated in glioma, and high-level of TRPV4 indicates a worse prognosis.•TRPV4 activation enhances the cell migration and invasion of glioma.•TRPV4-induced cell motility via AKT/Rac1 signaling pathway. |
| doi_str_mv | 10.1016/j.bbrc.2018.06.090 |
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•TRPV4 is upregulated in glioma, and high-level of TRPV4 indicates a worse prognosis.•TRPV4 activation enhances the cell migration and invasion of glioma.•TRPV4-induced cell motility via AKT/Rac1 signaling pathway.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2018.06.090</identifier><identifier>PMID: 29928875</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; agonists ; AKT ; antagonists ; Blotting, Western ; botulinum toxin ; Cell Line, Tumor ; Cell Movement ; Glioma ; Glioma - metabolism ; Glioma - pathology ; GLIOMAS ; Humans ; Invasion ; Leucine - analogs & derivatives ; Leucine - pharmacology ; migratory behavior ; Morpholines - pharmacology ; Neoplasm Invasiveness ; PHOSPHORYLATION ; prognosis ; Proto-Oncogene Proteins c-akt - metabolism ; Pyrroles - pharmacology ; Rac1 ; rac1 GTP-Binding Protein - metabolism ; RECEPTORS ; Signal Transduction ; Sulfonamides - pharmacology ; therapeutics ; THERAPY ; TOXINS ; transient receptor potential vanilloid channels ; TRPV Cation Channels - agonists ; TRPV Cation Channels - antagonists & inhibitors ; TRPV Cation Channels - metabolism ; TRPV4</subject><ispartof>Biochemical and biophysical research communications, 2018-09, Vol.503 (2), p.876-881</ispartof><rights>2018 Elsevier Inc.</rights><rights>Copyright © 2018 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-e833810794ed30748705e3e043a79b09d4ff85e4ba19e923e92bbb17585af453</citedby><cites>FETCH-LOGICAL-c483t-e833810794ed30748705e3e043a79b09d4ff85e4ba19e923e92bbb17585af453</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X18314025$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29928875$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/23136922$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Ou-yang, Qing</creatorcontrib><creatorcontrib>Li, Bing</creatorcontrib><creatorcontrib>Xu, Minhui</creatorcontrib><creatorcontrib>Liang, Hong</creatorcontrib><title>TRPV4 promotes the migration and invasion of glioma cells via AKT/Rac1 signaling</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Experimental evidence indicates a critical role of TRPV4 (Transient Receptor Potential Vanilloid 4) in controlling the cell migratory activity of multiple tumors. However, the oncogenic role of TRPV4 in glioma still remains elusive. In this study, we tried to investigate the oncogenic role of TRPV4 in glioma. We found that the expression levels of TRPV4 were upregulated in glioma and the high levels of TRPV4 indicated a worse prognosis in patients with glioma. TRPV4 was critical for glioma migration and invasion: activating TRPV4 by agonist GSK1016790 A enhanced glioma migration and invasion, while, the specific TRPV4 antagonist HC-067047 suppressed glioma migration and invasion. Mechanically, activated TRPV4 promoted the activation of Rac1 (Ras-related C3 botulinum toxin substrate 1) by targeting the AKT for phosphorylation, then enhanced glioma migration and invasion. All these results suggested that TRPV4 accelerates glioma migration and invasion through the AKT/Rac1 signaling, and TRPV4 might be considered as a potential target for glioma therapy.
•TRPV4 is upregulated in glioma, and high-level of TRPV4 indicates a worse prognosis.•TRPV4 activation enhances the cell migration and invasion of glioma.•TRPV4-induced cell motility via AKT/Rac1 signaling pathway.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>agonists</subject><subject>AKT</subject><subject>antagonists</subject><subject>Blotting, Western</subject><subject>botulinum toxin</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Glioma</subject><subject>Glioma - metabolism</subject><subject>Glioma - pathology</subject><subject>GLIOMAS</subject><subject>Humans</subject><subject>Invasion</subject><subject>Leucine - analogs & derivatives</subject><subject>Leucine - pharmacology</subject><subject>migratory behavior</subject><subject>Morpholines - pharmacology</subject><subject>Neoplasm Invasiveness</subject><subject>PHOSPHORYLATION</subject><subject>prognosis</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Pyrroles - pharmacology</subject><subject>Rac1</subject><subject>rac1 GTP-Binding Protein - metabolism</subject><subject>RECEPTORS</subject><subject>Signal Transduction</subject><subject>Sulfonamides - pharmacology</subject><subject>therapeutics</subject><subject>THERAPY</subject><subject>TOXINS</subject><subject>transient receptor potential vanilloid channels</subject><subject>TRPV Cation Channels - agonists</subject><subject>TRPV Cation Channels - antagonists & inhibitors</subject><subject>TRPV Cation Channels - metabolism</subject><subject>TRPV4</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU-LFDEQxYMo7uzqF_AgAS9eurfyp7sT8LIs6ooLLssg3kI6XT2boTtZk54Bv71pZvUoHkIR-NWrevUIecOgZsDay33d98nVHJiqoa1BwzOyYaVUnIF8TjYA0FZcsx9n5DznPQBjstUvyRnXmivVNRtyt72_-y7pY4pzXDDT5QHp7HfJLj4GasNAfTjavH7iSHeTj7OlDqcp06O39Orr9vLeOkaz3wU7-bB7RV6Mdsr4-qlekO2nj9vrm-r22-cv11e3lZNKLBUqIRSDTkscBHRSddCgQJDCdroHPchxVA3K3jKNmovy-r5nXaMaO8pGXJB3J9mYF2-y8wu6BxdDQLcYLphoNeeFen-iir-fB8yLmX1et7cB4yEbzgRTrRT6P1Aoo8vVYZ3NT6hLMeeEo3lMfrbpl2Fg1mTM3qzJmDUZA60pkZSmt0_6h37G4W_LnygK8OEEYLna0WNaXWFwOPi0mhqi_5f-b2Y3nCI</recordid><startdate>20180905</startdate><enddate>20180905</enddate><creator>Ou-yang, Qing</creator><creator>Li, Bing</creator><creator>Xu, Minhui</creator><creator>Liang, Hong</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>7S9</scope><scope>L.6</scope><scope>OTOTI</scope></search><sort><creationdate>20180905</creationdate><title>TRPV4 promotes the migration and invasion of glioma cells via AKT/Rac1 signaling</title><author>Ou-yang, Qing ; Li, Bing ; Xu, Minhui ; Liang, Hong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-e833810794ed30748705e3e043a79b09d4ff85e4ba19e923e92bbb17585af453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>agonists</topic><topic>AKT</topic><topic>antagonists</topic><topic>Blotting, Western</topic><topic>botulinum toxin</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Glioma</topic><topic>Glioma - metabolism</topic><topic>Glioma - pathology</topic><topic>GLIOMAS</topic><topic>Humans</topic><topic>Invasion</topic><topic>Leucine - analogs & derivatives</topic><topic>Leucine - pharmacology</topic><topic>migratory behavior</topic><topic>Morpholines - pharmacology</topic><topic>Neoplasm Invasiveness</topic><topic>PHOSPHORYLATION</topic><topic>prognosis</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Pyrroles - pharmacology</topic><topic>Rac1</topic><topic>rac1 GTP-Binding Protein - metabolism</topic><topic>RECEPTORS</topic><topic>Signal Transduction</topic><topic>Sulfonamides - pharmacology</topic><topic>therapeutics</topic><topic>THERAPY</topic><topic>TOXINS</topic><topic>transient receptor potential vanilloid channels</topic><topic>TRPV Cation Channels - agonists</topic><topic>TRPV Cation Channels - antagonists & inhibitors</topic><topic>TRPV Cation Channels - metabolism</topic><topic>TRPV4</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ou-yang, Qing</creatorcontrib><creatorcontrib>Li, Bing</creatorcontrib><creatorcontrib>Xu, Minhui</creatorcontrib><creatorcontrib>Liang, Hong</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>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>OSTI.GOV</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ou-yang, Qing</au><au>Li, Bing</au><au>Xu, Minhui</au><au>Liang, Hong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TRPV4 promotes the migration and invasion of glioma cells via AKT/Rac1 signaling</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2018-09-05</date><risdate>2018</risdate><volume>503</volume><issue>2</issue><spage>876</spage><epage>881</epage><pages>876-881</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Experimental evidence indicates a critical role of TRPV4 (Transient Receptor Potential Vanilloid 4) in controlling the cell migratory activity of multiple tumors. However, the oncogenic role of TRPV4 in glioma still remains elusive. In this study, we tried to investigate the oncogenic role of TRPV4 in glioma. We found that the expression levels of TRPV4 were upregulated in glioma and the high levels of TRPV4 indicated a worse prognosis in patients with glioma. TRPV4 was critical for glioma migration and invasion: activating TRPV4 by agonist GSK1016790 A enhanced glioma migration and invasion, while, the specific TRPV4 antagonist HC-067047 suppressed glioma migration and invasion. Mechanically, activated TRPV4 promoted the activation of Rac1 (Ras-related C3 botulinum toxin substrate 1) by targeting the AKT for phosphorylation, then enhanced glioma migration and invasion. All these results suggested that TRPV4 accelerates glioma migration and invasion through the AKT/Rac1 signaling, and TRPV4 might be considered as a potential target for glioma therapy.
•TRPV4 is upregulated in glioma, and high-level of TRPV4 indicates a worse prognosis.•TRPV4 activation enhances the cell migration and invasion of glioma.•TRPV4-induced cell motility via AKT/Rac1 signaling pathway.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>29928875</pmid><doi>10.1016/j.bbrc.2018.06.090</doi><tpages>6</tpages></addata></record> |
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| subjects | 60 APPLIED LIFE SCIENCES agonists AKT antagonists Blotting, Western botulinum toxin Cell Line, Tumor Cell Movement Glioma Glioma - metabolism Glioma - pathology GLIOMAS Humans Invasion Leucine - analogs & derivatives Leucine - pharmacology migratory behavior Morpholines - pharmacology Neoplasm Invasiveness PHOSPHORYLATION prognosis Proto-Oncogene Proteins c-akt - metabolism Pyrroles - pharmacology Rac1 rac1 GTP-Binding Protein - metabolism RECEPTORS Signal Transduction Sulfonamides - pharmacology therapeutics THERAPY TOXINS transient receptor potential vanilloid channels TRPV Cation Channels - agonists TRPV Cation Channels - antagonists & inhibitors TRPV Cation Channels - metabolism TRPV4 |
| title | TRPV4 promotes the migration and invasion of glioma cells via AKT/Rac1 signaling |
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