Targeting the centriolar replication factor STIL synergizes with DNA damaging agents for treatment of ovarian cancer
Advanced ovarian cancer is an incurable disease. Thus, novel therapies are required. We wished to identify new therapeutic targets for ovarian cancer. ShRNA screen performed in 42 ovarian cancer cell lines identified the centriolar replication factor STIL as an essential gene for ovarian cancer cell...
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| Veröffentlicht in: | Oncotarget 2017-04, Vol.8 (16), p.27380-27392 |
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| creator | Rabinowicz, Noa Mangala, Lingegowda S Brown, Kevin R Checa-Rodriguez, Cintia Castiel, Asher Moskovich, Oren Zarfati, Giulia Trakhtenbrot, Luba Levy-Barda, Adva Jiang, Dahai Rodriguez-Aguayo, Cristian Pradeep, Sunila van Praag, Yael Lopez-Berestein, Gabriel David, Ahuvit Novikov, Ilya Huertas, Pablo Rottapel, Robert Sood, Anil K Izraeli, Shai |
| description | Advanced ovarian cancer is an incurable disease. Thus, novel therapies are required. We wished to identify new therapeutic targets for ovarian cancer. ShRNA screen performed in 42 ovarian cancer cell lines identified the centriolar replication factor STIL as an essential gene for ovarian cancer cells. This was verified in-vivo in orthotopic human ovarian cancer mouse models. STIL depletion by administration of siRNA in neutral liposomes resulted in robust anti-tumor effect that was further enhanced in combination with cisplatin. Consistent with this finding, STIL depletion enhanced the extent of DNA double strand breaks caused by DNA damaging agents. This was associated with centrosomal depletion, ongoing genomic instability and enhanced formation of micronuclei. Interestingly, the ongoing DNA damage was not associated with reduced DNA repair. Indeed, we observed that depletion of STIL enhanced canonical homologous recombination repair and increased BRCA1 and RAD51 foci in response to DNA double strand breaks. Thus, inhibition of STIL significantly enhances the efficacy of DNA damaging chemotherapeutic drugs in treatment of ovarian cancer. |
| doi_str_mv | 10.18632/oncotarget.16068 |
| format | Article |
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Thus, novel therapies are required. We wished to identify new therapeutic targets for ovarian cancer. ShRNA screen performed in 42 ovarian cancer cell lines identified the centriolar replication factor STIL as an essential gene for ovarian cancer cells. This was verified in-vivo in orthotopic human ovarian cancer mouse models. STIL depletion by administration of siRNA in neutral liposomes resulted in robust anti-tumor effect that was further enhanced in combination with cisplatin. Consistent with this finding, STIL depletion enhanced the extent of DNA double strand breaks caused by DNA damaging agents. This was associated with centrosomal depletion, ongoing genomic instability and enhanced formation of micronuclei. Interestingly, the ongoing DNA damage was not associated with reduced DNA repair. Indeed, we observed that depletion of STIL enhanced canonical homologous recombination repair and increased BRCA1 and RAD51 foci in response to DNA double strand breaks. Thus, inhibition of STIL significantly enhances the efficacy of DNA damaging chemotherapeutic drugs in treatment of ovarian cancer.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.16068</identifier><identifier>PMID: 28423708</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>Animals ; Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Cell Cycle - drug effects ; Cell Cycle - genetics ; Cell Line, Tumor ; Cell Survival - drug effects ; Cell Survival - genetics ; Disease Models, Animal ; DNA Breaks, Double-Stranded ; DNA Damage - drug effects ; DNA Repair ; Dose-Response Relationship, Drug ; Female ; Histones - metabolism ; Humans ; Intracellular Signaling Peptides and Proteins - antagonists & inhibitors ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - metabolism ; Mice ; Molecular Targeted Therapy ; Ovarian Neoplasms - drug therapy ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - metabolism ; Ovarian Neoplasms - pathology ; Recombinational DNA Repair ; Research Paper ; RNA Interference ; RNA, Small Interfering - genetics ; Signal Transduction ; Tumor Suppressor p53-Binding Protein 1 - metabolism ; Xenograft Model Antitumor Assays</subject><ispartof>Oncotarget, 2017-04, Vol.8 (16), p.27380-27392</ispartof><rights>Copyright: © 2017 Rabinowicz et al. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c399t-124a02f5a8f1dc86547a0445f87f78bf95f2cffec2da4beff6f038aaa7e7e57c3</citedby><cites>FETCH-LOGICAL-c399t-124a02f5a8f1dc86547a0445f87f78bf95f2cffec2da4beff6f038aaa7e7e57c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5432342/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5432342/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28423708$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rabinowicz, Noa</creatorcontrib><creatorcontrib>Mangala, Lingegowda S</creatorcontrib><creatorcontrib>Brown, Kevin R</creatorcontrib><creatorcontrib>Checa-Rodriguez, Cintia</creatorcontrib><creatorcontrib>Castiel, Asher</creatorcontrib><creatorcontrib>Moskovich, Oren</creatorcontrib><creatorcontrib>Zarfati, Giulia</creatorcontrib><creatorcontrib>Trakhtenbrot, Luba</creatorcontrib><creatorcontrib>Levy-Barda, Adva</creatorcontrib><creatorcontrib>Jiang, Dahai</creatorcontrib><creatorcontrib>Rodriguez-Aguayo, Cristian</creatorcontrib><creatorcontrib>Pradeep, Sunila</creatorcontrib><creatorcontrib>van Praag, Yael</creatorcontrib><creatorcontrib>Lopez-Berestein, Gabriel</creatorcontrib><creatorcontrib>David, Ahuvit</creatorcontrib><creatorcontrib>Novikov, Ilya</creatorcontrib><creatorcontrib>Huertas, Pablo</creatorcontrib><creatorcontrib>Rottapel, Robert</creatorcontrib><creatorcontrib>Sood, Anil K</creatorcontrib><creatorcontrib>Izraeli, Shai</creatorcontrib><title>Targeting the centriolar replication factor STIL synergizes with DNA damaging agents for treatment of ovarian cancer</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>Advanced ovarian cancer is an incurable disease. Thus, novel therapies are required. We wished to identify new therapeutic targets for ovarian cancer. ShRNA screen performed in 42 ovarian cancer cell lines identified the centriolar replication factor STIL as an essential gene for ovarian cancer cells. This was verified in-vivo in orthotopic human ovarian cancer mouse models. STIL depletion by administration of siRNA in neutral liposomes resulted in robust anti-tumor effect that was further enhanced in combination with cisplatin. Consistent with this finding, STIL depletion enhanced the extent of DNA double strand breaks caused by DNA damaging agents. This was associated with centrosomal depletion, ongoing genomic instability and enhanced formation of micronuclei. Interestingly, the ongoing DNA damage was not associated with reduced DNA repair. Indeed, we observed that depletion of STIL enhanced canonical homologous recombination repair and increased BRCA1 and RAD51 foci in response to DNA double strand breaks. Thus, inhibition of STIL significantly enhances the efficacy of DNA damaging chemotherapeutic drugs in treatment of ovarian cancer.</description><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Cycle - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - genetics</subject><subject>Disease Models, Animal</subject><subject>DNA Breaks, Double-Stranded</subject><subject>DNA Damage - drug effects</subject><subject>DNA Repair</subject><subject>Dose-Response Relationship, Drug</subject><subject>Female</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - antagonists & inhibitors</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Mice</subject><subject>Molecular Targeted Therapy</subject><subject>Ovarian Neoplasms - drug therapy</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Recombinational DNA Repair</subject><subject>Research Paper</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - genetics</subject><subject>Signal Transduction</subject><subject>Tumor Suppressor p53-Binding Protein 1 - metabolism</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1949-2553</issn><issn>1949-2553</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkctOwzAQRS0EolXpB7BB_oEUP_JwNkhVeVWqYEFZW1PHTo2SuHJMUfl6QgqlzMYzsu-Z8VyELimZUJFydu0a5QL4UocJTUkqTtCQ5nEesSThp0f5AI3b9o10kcSZYPk5GjARM54RMURh2RNsU-Kw1ljpJnjrKvDY601lFQTrGmxABefxy3K-wO2u0b60n7rFHzas8e3TFBdQQ_nNgLIDtNh0j4PXEOquxM5gtwVvocEKGqX9BTozULV6_HOO0Ov93XL2GC2eH-az6SJSPM9DRFkMhJkEhKGFEmk3PpA4TozITCZWJk8MU8ZoxQqIV9qY1BAuACDTmU4yxUfoZs_dvK9qXfSfg0puvK3B76QDK__fNHYtS7eVScwZ71Y0QnQPUN61rdfmoKVE9i7IPxdk70KnuTpuelD87px_AYLKisE</recordid><startdate>20170418</startdate><enddate>20170418</enddate><creator>Rabinowicz, Noa</creator><creator>Mangala, Lingegowda S</creator><creator>Brown, Kevin R</creator><creator>Checa-Rodriguez, Cintia</creator><creator>Castiel, Asher</creator><creator>Moskovich, Oren</creator><creator>Zarfati, Giulia</creator><creator>Trakhtenbrot, Luba</creator><creator>Levy-Barda, Adva</creator><creator>Jiang, Dahai</creator><creator>Rodriguez-Aguayo, Cristian</creator><creator>Pradeep, Sunila</creator><creator>van Praag, Yael</creator><creator>Lopez-Berestein, Gabriel</creator><creator>David, Ahuvit</creator><creator>Novikov, Ilya</creator><creator>Huertas, Pablo</creator><creator>Rottapel, Robert</creator><creator>Sood, Anil K</creator><creator>Izraeli, Shai</creator><general>Impact Journals LLC</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>5PM</scope></search><sort><creationdate>20170418</creationdate><title>Targeting the centriolar replication factor STIL synergizes with DNA damaging agents for treatment of ovarian cancer</title><author>Rabinowicz, Noa ; 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Thus, novel therapies are required. We wished to identify new therapeutic targets for ovarian cancer. ShRNA screen performed in 42 ovarian cancer cell lines identified the centriolar replication factor STIL as an essential gene for ovarian cancer cells. This was verified in-vivo in orthotopic human ovarian cancer mouse models. STIL depletion by administration of siRNA in neutral liposomes resulted in robust anti-tumor effect that was further enhanced in combination with cisplatin. Consistent with this finding, STIL depletion enhanced the extent of DNA double strand breaks caused by DNA damaging agents. This was associated with centrosomal depletion, ongoing genomic instability and enhanced formation of micronuclei. Interestingly, the ongoing DNA damage was not associated with reduced DNA repair. Indeed, we observed that depletion of STIL enhanced canonical homologous recombination repair and increased BRCA1 and RAD51 foci in response to DNA double strand breaks. Thus, inhibition of STIL significantly enhances the efficacy of DNA damaging chemotherapeutic drugs in treatment of ovarian cancer.</abstract><cop>United States</cop><pub>Impact Journals LLC</pub><pmid>28423708</pmid><doi>10.18632/oncotarget.16068</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Cell Cycle - drug effects Cell Cycle - genetics Cell Line, Tumor Cell Survival - drug effects Cell Survival - genetics Disease Models, Animal DNA Breaks, Double-Stranded DNA Damage - drug effects DNA Repair Dose-Response Relationship, Drug Female Histones - metabolism Humans Intracellular Signaling Peptides and Proteins - antagonists & inhibitors Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Mice Molecular Targeted Therapy Ovarian Neoplasms - drug therapy Ovarian Neoplasms - genetics Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Recombinational DNA Repair Research Paper RNA Interference RNA, Small Interfering - genetics Signal Transduction Tumor Suppressor p53-Binding Protein 1 - metabolism Xenograft Model Antitumor Assays |
| title | Targeting the centriolar replication factor STIL synergizes with DNA damaging agents for treatment of ovarian cancer |
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