Poly (ADP) Ribose Glycohydrolase Can Be Effectively Targeted in Pancreatic Cancer
Patients with metastatic pancreatic ductal adenocarcinoma (PDAC) have an average survival of less than 1 year, underscoring the importance of evaluating novel targets with matched targeted agents. We recently identified that poly (ADP) ribose glycohydrolase (PARG) is a strong candidate target due to...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2019-09, Vol.79 (17), p.4491-4502 |
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| creator | Jain, Aditi Agostini, Lebaron C McCarthy, Grace A Chand, Saswati N Ramirez, AnnJosette Nevler, Avinoam Cozzitorto, Joseph Schultz, Christopher W Lowder, Cinthya Yabar Smith, Kate M Waddell, Ian D Raitses-Gurevich, Maria Stossel, Chani Gorman, Yulia Glick Atias, Dikla Yeo, Charles J Winter, Jordan M Olive, Kenneth P Golan, Talia Pishvaian, Michael J Ogilvie, Donald James, Dominic I Jordan, Allan M Brody, Jonathan R |
| description | Patients with metastatic pancreatic ductal adenocarcinoma (PDAC) have an average survival of less than 1 year, underscoring the importance of evaluating novel targets with matched targeted agents. We recently identified that poly (ADP) ribose glycohydrolase (PARG) is a strong candidate target due to its dependence on the pro-oncogenic mRNA stability factor HuR (
). Here, we evaluated PARG as a target in PDAC models using both genetic silencing of PARG and established small-molecule PARG inhibitors (PARGi), PDDX-01/04. Homologous repair-deficient cells compared with homologous repair-proficient cells were more sensitive to PARGi
.
, silencing of PARG significantly decreased tumor growth. PARGi synergized with DNA-damaging agents (i.e., oxaliplatin and 5-fluorouracil), but not with PARPi therapy. Mechanistically, combined PARGi and oxaliplatin treatment led to persistence of detrimental PARylation, increased expression of cleaved caspase-3, and increased γH2AX foci. In summary, these data validate PARG as a relevant target in PDAC and establish current therapies that synergize with PARGi. SIGNIFICANCE: PARG is a potential target in pancreatic cancer as a single-agent anticancer therapy or in combination with current standard of care. |
| doi_str_mv | 10.1158/0008-5472.CAN-18-3645 |
| format | Article |
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). Here, we evaluated PARG as a target in PDAC models using both genetic silencing of PARG and established small-molecule PARG inhibitors (PARGi), PDDX-01/04. Homologous repair-deficient cells compared with homologous repair-proficient cells were more sensitive to PARGi
.
, silencing of PARG significantly decreased tumor growth. PARGi synergized with DNA-damaging agents (i.e., oxaliplatin and 5-fluorouracil), but not with PARPi therapy. Mechanistically, combined PARGi and oxaliplatin treatment led to persistence of detrimental PARylation, increased expression of cleaved caspase-3, and increased γH2AX foci. In summary, these data validate PARG as a relevant target in PDAC and establish current therapies that synergize with PARGi. SIGNIFICANCE: PARG is a potential target in pancreatic cancer as a single-agent anticancer therapy or in combination with current standard of care.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-18-3645</identifier><identifier>PMID: 31273064</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Carcinoma, Pancreatic Ductal - drug therapy ; Carcinoma, Pancreatic Ductal - genetics ; Carcinoma, Pancreatic Ductal - pathology ; Cell Line, Tumor ; DNA Damage ; Enzyme Inhibitors - pharmacology ; Female ; Gene Silencing ; Glycoside Hydrolases - antagonists & inhibitors ; Glycoside Hydrolases - genetics ; Humans ; Mice, Nude ; Molecular Targeted Therapy ; Oxaliplatin - pharmacology ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - pathology ; Recombinational DNA Repair ; Small Molecule Libraries - pharmacology ; Xenograft Model Antitumor Assays</subject><ispartof>Cancer research (Chicago, Ill.), 2019-09, Vol.79 (17), p.4491-4502</ispartof><rights>2019 American Association for Cancer Research.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-70066d0611cdeeb34c4c8f9c2bfacaa82cd185441167776cbf238c18363c5c7f3</citedby><cites>FETCH-LOGICAL-c463t-70066d0611cdeeb34c4c8f9c2bfacaa82cd185441167776cbf238c18363c5c7f3</cites><orcidid>0000-0001-5625-0517 ; 0000-0002-5928-0559 ; 0000-0003-3362-025X ; 0000-0003-4578-6011 ; 0000-0001-5731-2847</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3343,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31273064$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jain, Aditi</creatorcontrib><creatorcontrib>Agostini, Lebaron C</creatorcontrib><creatorcontrib>McCarthy, Grace A</creatorcontrib><creatorcontrib>Chand, Saswati N</creatorcontrib><creatorcontrib>Ramirez, AnnJosette</creatorcontrib><creatorcontrib>Nevler, Avinoam</creatorcontrib><creatorcontrib>Cozzitorto, Joseph</creatorcontrib><creatorcontrib>Schultz, Christopher W</creatorcontrib><creatorcontrib>Lowder, Cinthya Yabar</creatorcontrib><creatorcontrib>Smith, Kate M</creatorcontrib><creatorcontrib>Waddell, Ian D</creatorcontrib><creatorcontrib>Raitses-Gurevich, Maria</creatorcontrib><creatorcontrib>Stossel, Chani</creatorcontrib><creatorcontrib>Gorman, Yulia Glick</creatorcontrib><creatorcontrib>Atias, Dikla</creatorcontrib><creatorcontrib>Yeo, Charles J</creatorcontrib><creatorcontrib>Winter, Jordan M</creatorcontrib><creatorcontrib>Olive, Kenneth P</creatorcontrib><creatorcontrib>Golan, Talia</creatorcontrib><creatorcontrib>Pishvaian, Michael J</creatorcontrib><creatorcontrib>Ogilvie, Donald</creatorcontrib><creatorcontrib>James, Dominic I</creatorcontrib><creatorcontrib>Jordan, Allan M</creatorcontrib><creatorcontrib>Brody, Jonathan R</creatorcontrib><title>Poly (ADP) Ribose Glycohydrolase Can Be Effectively Targeted in Pancreatic Cancer</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Patients with metastatic pancreatic ductal adenocarcinoma (PDAC) have an average survival of less than 1 year, underscoring the importance of evaluating novel targets with matched targeted agents. We recently identified that poly (ADP) ribose glycohydrolase (PARG) is a strong candidate target due to its dependence on the pro-oncogenic mRNA stability factor HuR (
). Here, we evaluated PARG as a target in PDAC models using both genetic silencing of PARG and established small-molecule PARG inhibitors (PARGi), PDDX-01/04. Homologous repair-deficient cells compared with homologous repair-proficient cells were more sensitive to PARGi
.
, silencing of PARG significantly decreased tumor growth. PARGi synergized with DNA-damaging agents (i.e., oxaliplatin and 5-fluorouracil), but not with PARPi therapy. Mechanistically, combined PARGi and oxaliplatin treatment led to persistence of detrimental PARylation, increased expression of cleaved caspase-3, and increased γH2AX foci. In summary, these data validate PARG as a relevant target in PDAC and establish current therapies that synergize with PARGi. SIGNIFICANCE: PARG is a potential target in pancreatic cancer as a single-agent anticancer therapy or in combination with current standard of care.</description><subject>Animals</subject><subject>Carcinoma, Pancreatic Ductal - drug therapy</subject><subject>Carcinoma, Pancreatic Ductal - genetics</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Cell Line, Tumor</subject><subject>DNA Damage</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Female</subject><subject>Gene Silencing</subject><subject>Glycoside Hydrolases - antagonists & inhibitors</subject><subject>Glycoside Hydrolases - genetics</subject><subject>Humans</subject><subject>Mice, Nude</subject><subject>Molecular Targeted Therapy</subject><subject>Oxaliplatin - pharmacology</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Recombinational DNA Repair</subject><subject>Small Molecule Libraries - pharmacology</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkVtLw0AQhRdRtFZ_gpLH-pC6m71k-yLUWi8gWqU-L5vJpEbSbN1NC_33JqhFn4ZhvjkznEPIGaNDxqS-pJTqWIo0GU7GTzHTMVdC7pEek1zHqRByn_R2zBE5DuGjbSWj8pAccZaknCrRIy8zV22jwfhmdhG9lpkLGN1VW3Dv29y7yrbtxNbRNUbTokBoyg22-Nz6BTaYR2UdzWwNHm1TQkcC-hNyUNgq4OlP7ZO32-l8ch8_Pt89TMaPMQjFmzilVKmcKsYgR8y4AAG6GEGSFRas1QnkTEshGFNpmirIioRrYJorDhLSgvfJ1bfuap0tMQesG28rs_Ll0vqtcbY0_yd1-W4WbmOUZkpS1QoMfgS8-1xjaMyyDIBVZWt062CSRPJEjVrLWlR-o-BdCB6L3RlGTReH6aw2ndWmjcMwbbo42r3zvz_utn7951_fi4Yc</recordid><startdate>20190901</startdate><enddate>20190901</enddate><creator>Jain, Aditi</creator><creator>Agostini, Lebaron C</creator><creator>McCarthy, Grace A</creator><creator>Chand, Saswati N</creator><creator>Ramirez, AnnJosette</creator><creator>Nevler, Avinoam</creator><creator>Cozzitorto, Joseph</creator><creator>Schultz, Christopher W</creator><creator>Lowder, Cinthya Yabar</creator><creator>Smith, Kate M</creator><creator>Waddell, Ian D</creator><creator>Raitses-Gurevich, Maria</creator><creator>Stossel, Chani</creator><creator>Gorman, Yulia Glick</creator><creator>Atias, Dikla</creator><creator>Yeo, Charles J</creator><creator>Winter, Jordan M</creator><creator>Olive, Kenneth P</creator><creator>Golan, Talia</creator><creator>Pishvaian, Michael J</creator><creator>Ogilvie, Donald</creator><creator>James, Dominic I</creator><creator>Jordan, Allan M</creator><creator>Brody, Jonathan R</creator><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>5PM</scope><orcidid>https://orcid.org/0000-0001-5625-0517</orcidid><orcidid>https://orcid.org/0000-0002-5928-0559</orcidid><orcidid>https://orcid.org/0000-0003-3362-025X</orcidid><orcidid>https://orcid.org/0000-0003-4578-6011</orcidid><orcidid>https://orcid.org/0000-0001-5731-2847</orcidid></search><sort><creationdate>20190901</creationdate><title>Poly (ADP) Ribose Glycohydrolase Can Be Effectively Targeted in Pancreatic Cancer</title><author>Jain, Aditi ; Agostini, Lebaron C ; McCarthy, Grace A ; Chand, Saswati N ; Ramirez, AnnJosette ; Nevler, Avinoam ; Cozzitorto, Joseph ; Schultz, Christopher W ; Lowder, Cinthya Yabar ; Smith, Kate M ; Waddell, Ian D ; Raitses-Gurevich, Maria ; Stossel, Chani ; Gorman, Yulia Glick ; Atias, Dikla ; Yeo, Charles J ; Winter, Jordan M ; Olive, Kenneth P ; Golan, Talia ; Pishvaian, Michael J ; Ogilvie, Donald ; James, Dominic I ; Jordan, Allan M ; Brody, Jonathan R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-70066d0611cdeeb34c4c8f9c2bfacaa82cd185441167776cbf238c18363c5c7f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Carcinoma, Pancreatic Ductal - drug therapy</topic><topic>Carcinoma, Pancreatic Ductal - genetics</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Cell Line, Tumor</topic><topic>DNA Damage</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Female</topic><topic>Gene Silencing</topic><topic>Glycoside Hydrolases - antagonists & inhibitors</topic><topic>Glycoside Hydrolases - genetics</topic><topic>Humans</topic><topic>Mice, Nude</topic><topic>Molecular Targeted Therapy</topic><topic>Oxaliplatin - pharmacology</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Recombinational DNA Repair</topic><topic>Small Molecule Libraries - pharmacology</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jain, Aditi</creatorcontrib><creatorcontrib>Agostini, Lebaron C</creatorcontrib><creatorcontrib>McCarthy, Grace A</creatorcontrib><creatorcontrib>Chand, Saswati N</creatorcontrib><creatorcontrib>Ramirez, AnnJosette</creatorcontrib><creatorcontrib>Nevler, Avinoam</creatorcontrib><creatorcontrib>Cozzitorto, Joseph</creatorcontrib><creatorcontrib>Schultz, Christopher W</creatorcontrib><creatorcontrib>Lowder, Cinthya Yabar</creatorcontrib><creatorcontrib>Smith, Kate M</creatorcontrib><creatorcontrib>Waddell, Ian D</creatorcontrib><creatorcontrib>Raitses-Gurevich, Maria</creatorcontrib><creatorcontrib>Stossel, Chani</creatorcontrib><creatorcontrib>Gorman, Yulia Glick</creatorcontrib><creatorcontrib>Atias, Dikla</creatorcontrib><creatorcontrib>Yeo, Charles J</creatorcontrib><creatorcontrib>Winter, Jordan M</creatorcontrib><creatorcontrib>Olive, Kenneth P</creatorcontrib><creatorcontrib>Golan, Talia</creatorcontrib><creatorcontrib>Pishvaian, Michael J</creatorcontrib><creatorcontrib>Ogilvie, Donald</creatorcontrib><creatorcontrib>James, Dominic I</creatorcontrib><creatorcontrib>Jordan, Allan M</creatorcontrib><creatorcontrib>Brody, Jonathan R</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>PubMed Central (Full Participant titles)</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jain, Aditi</au><au>Agostini, Lebaron C</au><au>McCarthy, Grace A</au><au>Chand, Saswati N</au><au>Ramirez, AnnJosette</au><au>Nevler, Avinoam</au><au>Cozzitorto, Joseph</au><au>Schultz, Christopher W</au><au>Lowder, Cinthya Yabar</au><au>Smith, Kate M</au><au>Waddell, Ian D</au><au>Raitses-Gurevich, Maria</au><au>Stossel, Chani</au><au>Gorman, Yulia Glick</au><au>Atias, Dikla</au><au>Yeo, Charles J</au><au>Winter, Jordan M</au><au>Olive, Kenneth P</au><au>Golan, Talia</au><au>Pishvaian, Michael J</au><au>Ogilvie, Donald</au><au>James, Dominic I</au><au>Jordan, Allan M</au><au>Brody, Jonathan R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Poly (ADP) Ribose Glycohydrolase Can Be Effectively Targeted in Pancreatic Cancer</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2019-09-01</date><risdate>2019</risdate><volume>79</volume><issue>17</issue><spage>4491</spage><epage>4502</epage><pages>4491-4502</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><abstract>Patients with metastatic pancreatic ductal adenocarcinoma (PDAC) have an average survival of less than 1 year, underscoring the importance of evaluating novel targets with matched targeted agents. We recently identified that poly (ADP) ribose glycohydrolase (PARG) is a strong candidate target due to its dependence on the pro-oncogenic mRNA stability factor HuR (
). Here, we evaluated PARG as a target in PDAC models using both genetic silencing of PARG and established small-molecule PARG inhibitors (PARGi), PDDX-01/04. Homologous repair-deficient cells compared with homologous repair-proficient cells were more sensitive to PARGi
.
, silencing of PARG significantly decreased tumor growth. PARGi synergized with DNA-damaging agents (i.e., oxaliplatin and 5-fluorouracil), but not with PARPi therapy. Mechanistically, combined PARGi and oxaliplatin treatment led to persistence of detrimental PARylation, increased expression of cleaved caspase-3, and increased γH2AX foci. In summary, these data validate PARG as a relevant target in PDAC and establish current therapies that synergize with PARGi. SIGNIFICANCE: PARG is a potential target in pancreatic cancer as a single-agent anticancer therapy or in combination with current standard of care.</abstract><cop>United States</cop><pmid>31273064</pmid><doi>10.1158/0008-5472.CAN-18-3645</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-5625-0517</orcidid><orcidid>https://orcid.org/0000-0002-5928-0559</orcidid><orcidid>https://orcid.org/0000-0003-3362-025X</orcidid><orcidid>https://orcid.org/0000-0003-4578-6011</orcidid><orcidid>https://orcid.org/0000-0001-5731-2847</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancer research (Chicago, Ill.), 2019-09, Vol.79 (17), p.4491-4502 |
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| source | MEDLINE; American Association for Cancer Research; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Carcinoma, Pancreatic Ductal - drug therapy Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - pathology Cell Line, Tumor DNA Damage Enzyme Inhibitors - pharmacology Female Gene Silencing Glycoside Hydrolases - antagonists & inhibitors Glycoside Hydrolases - genetics Humans Mice, Nude Molecular Targeted Therapy Oxaliplatin - pharmacology Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - pathology Recombinational DNA Repair Small Molecule Libraries - pharmacology Xenograft Model Antitumor Assays |
| title | Poly (ADP) Ribose Glycohydrolase Can Be Effectively Targeted in Pancreatic Cancer |
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