Pharmacological inhibition of Rho-kinase (ROCK) signaling enhances cisplatin resistance in neuroblastoma cells
The role of the RhoA/Rho kinase (ROCK) signaling pathway in cell survival remains a very controversial issue, with its activation being pro-apoptotic in many cell types and anti-apoptotic in others. To test if ROCK inhibition contributes to tumor cell survival or death following chemotherapy, we tre...
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| Veröffentlicht in: | International journal of oncology 2010-11, Vol.37 (5), p.1297-1305 |
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| container_issue | 5 |
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| container_title | International journal of oncology |
| container_volume | 37 |
| creator | STREET, Catharine A ROUTHIER, Alissa A SPENCER, Carrie PERKINS, Ashley L MASTERJOHN, Katherine HACKATHORN, Alexander MONTALVO, John DENNSTEDT, Emily A BRYAN, Brad A |
| description | The role of the RhoA/Rho kinase (ROCK) signaling pathway in cell survival remains a very controversial issue, with its activation being pro-apoptotic in many cell types and anti-apoptotic in others. To test if ROCK inhibition contributes to tumor cell survival or death following chemotherapy, we treated cisplatin damaged neuroblastoma cells with a pharmacological ROCK inhibitor (Y27632) or sham, and monitored cell survival, accumulation of a chemoresistant phenotype, and in vivo tumor formation. Additionally, we assayed if ROCK inhibition altered the expression of genes known to be involved in cisplatin resistance. Our studies indicate that ROCK inhibition results in increased cell survival, acquired chemoresistance, and enhanced tumor survival following cisplatin cytotoxicity, due in part to altered expression of cisplatin resistance genes. These findings suggest that ROCK inhibition in combination with cisplatin chemotherapy may lead to enhanced tumor chemoresistance in neuroblastoma. |
| doi_str_mv | 10.3892/ijo_00000781 |
| format | Article |
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To test if ROCK inhibition contributes to tumor cell survival or death following chemotherapy, we treated cisplatin damaged neuroblastoma cells with a pharmacological ROCK inhibitor (Y27632) or sham, and monitored cell survival, accumulation of a chemoresistant phenotype, and in vivo tumor formation. Additionally, we assayed if ROCK inhibition altered the expression of genes known to be involved in cisplatin resistance. Our studies indicate that ROCK inhibition results in increased cell survival, acquired chemoresistance, and enhanced tumor survival following cisplatin cytotoxicity, due in part to altered expression of cisplatin resistance genes. These findings suggest that ROCK inhibition in combination with cisplatin chemotherapy may lead to enhanced tumor chemoresistance in neuroblastoma.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo_00000781</identifier><identifier>PMID: 20878077</identifier><language>eng</language><publisher>Athens: Editorial Academy of the International Journal of Oncology</publisher><subject>Amides - pharmacology ; Antineoplastic Agents - pharmacology ; Biological and medical sciences ; Cell Line, Tumor ; Cell Survival - drug effects ; Cell Survival - physiology ; Cisplatin - pharmacology ; Drug Resistance, Neoplasm - genetics ; Enzyme Inhibitors - pharmacology ; Gene Expression - drug effects ; Humans ; Medical sciences ; Neuroblastoma - genetics ; Neuroblastoma - metabolism ; Neurology ; Pyridines - pharmacology ; rho-Associated Kinases - genetics ; rho-Associated Kinases - metabolism ; Signal Transduction - physiology ; Tumors ; Tumors of the nervous system. Phacomatoses</subject><ispartof>International journal of oncology, 2010-11, Vol.37 (5), p.1297-1305</ispartof><rights>2015 INIST-CNRS</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-a5cc23567b9b27f1f8e693395785c50d80a762b068d942949c16e003096b043e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23292412$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20878077$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>STREET, Catharine A</creatorcontrib><creatorcontrib>ROUTHIER, Alissa A</creatorcontrib><creatorcontrib>SPENCER, Carrie</creatorcontrib><creatorcontrib>PERKINS, Ashley L</creatorcontrib><creatorcontrib>MASTERJOHN, Katherine</creatorcontrib><creatorcontrib>HACKATHORN, Alexander</creatorcontrib><creatorcontrib>MONTALVO, John</creatorcontrib><creatorcontrib>DENNSTEDT, Emily A</creatorcontrib><creatorcontrib>BRYAN, Brad A</creatorcontrib><title>Pharmacological inhibition of Rho-kinase (ROCK) signaling enhances cisplatin resistance in neuroblastoma cells</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>The role of the RhoA/Rho kinase (ROCK) signaling pathway in cell survival remains a very controversial issue, with its activation being pro-apoptotic in many cell types and anti-apoptotic in others. To test if ROCK inhibition contributes to tumor cell survival or death following chemotherapy, we treated cisplatin damaged neuroblastoma cells with a pharmacological ROCK inhibitor (Y27632) or sham, and monitored cell survival, accumulation of a chemoresistant phenotype, and in vivo tumor formation. Additionally, we assayed if ROCK inhibition altered the expression of genes known to be involved in cisplatin resistance. Our studies indicate that ROCK inhibition results in increased cell survival, acquired chemoresistance, and enhanced tumor survival following cisplatin cytotoxicity, due in part to altered expression of cisplatin resistance genes. These findings suggest that ROCK inhibition in combination with cisplatin chemotherapy may lead to enhanced tumor chemoresistance in neuroblastoma.</description><subject>Amides - pharmacology</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - physiology</subject><subject>Cisplatin - pharmacology</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Gene Expression - drug effects</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Neuroblastoma - genetics</subject><subject>Neuroblastoma - metabolism</subject><subject>Neurology</subject><subject>Pyridines - pharmacology</subject><subject>rho-Associated Kinases - genetics</subject><subject>rho-Associated Kinases - metabolism</subject><subject>Signal Transduction - physiology</subject><subject>Tumors</subject><subject>Tumors of the nervous system. 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Phacomatoses</topic><toplevel>online_resources</toplevel><creatorcontrib>STREET, Catharine A</creatorcontrib><creatorcontrib>ROUTHIER, Alissa A</creatorcontrib><creatorcontrib>SPENCER, Carrie</creatorcontrib><creatorcontrib>PERKINS, Ashley L</creatorcontrib><creatorcontrib>MASTERJOHN, Katherine</creatorcontrib><creatorcontrib>HACKATHORN, Alexander</creatorcontrib><creatorcontrib>MONTALVO, John</creatorcontrib><creatorcontrib>DENNSTEDT, Emily A</creatorcontrib><creatorcontrib>BRYAN, Brad A</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>STREET, Catharine A</au><au>ROUTHIER, Alissa A</au><au>SPENCER, Carrie</au><au>PERKINS, Ashley L</au><au>MASTERJOHN, Katherine</au><au>HACKATHORN, Alexander</au><au>MONTALVO, John</au><au>DENNSTEDT, Emily A</au><au>BRYAN, Brad A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pharmacological inhibition of Rho-kinase (ROCK) signaling enhances cisplatin resistance in neuroblastoma cells</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2010-11-01</date><risdate>2010</risdate><volume>37</volume><issue>5</issue><spage>1297</spage><epage>1305</epage><pages>1297-1305</pages><issn>1019-6439</issn><eissn>1791-2423</eissn><abstract>The role of the RhoA/Rho kinase (ROCK) signaling pathway in cell survival remains a very controversial issue, with its activation being pro-apoptotic in many cell types and anti-apoptotic in others. 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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Amides - pharmacology Antineoplastic Agents - pharmacology Biological and medical sciences Cell Line, Tumor Cell Survival - drug effects Cell Survival - physiology Cisplatin - pharmacology Drug Resistance, Neoplasm - genetics Enzyme Inhibitors - pharmacology Gene Expression - drug effects Humans Medical sciences Neuroblastoma - genetics Neuroblastoma - metabolism Neurology Pyridines - pharmacology rho-Associated Kinases - genetics rho-Associated Kinases - metabolism Signal Transduction - physiology Tumors Tumors of the nervous system. Phacomatoses |
| title | Pharmacological inhibition of Rho-kinase (ROCK) signaling enhances cisplatin resistance in neuroblastoma cells |
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