The Significance of Targeting Poly (ADP-Ribose) Polymerase-1 in Pancreatic Cancer for Providing a New Therapeutic Paradigm
Genome-wide studies focusing on elucidating the effects on cancer progression have enabled the consequent identification of a distinct subpopulation of pancreatic cancer cells with unstable genomic characteristics. Based on this background, deleterious changes by poly (adenosine diphosphate (ADP)-ri...
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| Veröffentlicht in: | International journal of molecular sciences 2021-03, Vol.22 (7), p.3509 |
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| description | Genome-wide studies focusing on elucidating the effects on cancer progression have enabled the consequent identification of a distinct subpopulation of pancreatic cancer cells with unstable genomic characteristics. Based on this background, deleterious changes by poly (adenosine diphosphate (ADP)-ribose) polymerase-1 (PARP)-1 have been concentrated in oncology. One of the critical functions of PARP-1 is the response to DNA damage, which plays a pivotal role in DNA repair in cancers. PARP-1 also has widespread functions that are essential for the survival and growth of cancer cells. It regulates oxidative stress in mitochondria through the regulation of superoxide and oxidation. PARP-1 is in charge of regulating mitosis, which is a crucial role in tumorigenesis and remodels histones and chromatin enzymes related to transcriptional regulation, causing alterations in epigenetic markers and chromatin structure. Given the significance of these processes, it can be understood that these processes in cancer cells are at the frontline of the pathogenetic changes required for cancer cell survival, and these contributions can result in malignant transformation. Therefore, this review addresses the current molecular biological features for understanding the multifactorial function of PARP-1 in pancreatic cancer related to the aforementioned roles, along with the summary of recent approaches with PARP-1 inhibition in clinical studies targeting pancreatic cancer. This understanding could help to embrace the importance of targeting PARP-1 in the treatment of pancreatic cancer, which may present the potential to find out a variety of research topics that can be both challenged clinically and non-clinically. |
| doi_str_mv | 10.3390/ijms22073509 |
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Based on this background, deleterious changes by poly (adenosine diphosphate (ADP)-ribose) polymerase-1 (PARP)-1 have been concentrated in oncology. One of the critical functions of PARP-1 is the response to DNA damage, which plays a pivotal role in DNA repair in cancers. PARP-1 also has widespread functions that are essential for the survival and growth of cancer cells. It regulates oxidative stress in mitochondria through the regulation of superoxide and oxidation. PARP-1 is in charge of regulating mitosis, which is a crucial role in tumorigenesis and remodels histones and chromatin enzymes related to transcriptional regulation, causing alterations in epigenetic markers and chromatin structure. Given the significance of these processes, it can be understood that these processes in cancer cells are at the frontline of the pathogenetic changes required for cancer cell survival, and these contributions can result in malignant transformation. Therefore, this review addresses the current molecular biological features for understanding the multifactorial function of PARP-1 in pancreatic cancer related to the aforementioned roles, along with the summary of recent approaches with PARP-1 inhibition in clinical studies targeting pancreatic cancer. This understanding could help to embrace the importance of targeting PARP-1 in the treatment of pancreatic cancer, which may present the potential to find out a variety of research topics that can be both challenged clinically and non-clinically.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms22073509</identifier><identifier>PMID: 33805293</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adenosine ; Adenosine diphosphate ; Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Antioxidants ; Apoptosis ; Cancer therapies ; Cell cycle ; Chromatin ; Deoxyribonucleic acid ; DNA ; DNA Damage ; DNA Repair ; Drug resistance ; Enzymes ; Epigenetics ; Gene expression ; Gene regulation ; Genomes ; Histones ; Homeostasis ; Humans ; Hypoxia ; Kinases ; Metabolism ; Metabolites ; Mitochondria ; Mitosis ; Mutation ; Oxidation ; Oxidative Stress ; Pancreatic cancer ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - metabolism ; Pathogenesis ; Physiology ; Poly (ADP-Ribose) Polymerase-1 - antagonists & inhibitors ; Poly (ADP-Ribose) Polymerase-1 - metabolism ; Poly(ADP-ribose) polymerase ; Proteins ; Review ; Ribose ; Survival ; Transcription ; Transcription factors ; Transcription, Genetic ; Tumorigenesis</subject><ispartof>International journal of molecular sciences, 2021-03, Vol.22 (7), p.3509</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-42df90c952e4508e63b5d65d8be4438123aab745221c3cdfe3c360196c8a3a883</citedby><cites>FETCH-LOGICAL-c412t-42df90c952e4508e63b5d65d8be4438123aab745221c3cdfe3c360196c8a3a883</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/PMC8037971/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8037971/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33805293$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jeong, Keun-Yeong</creatorcontrib><creatorcontrib>Park, Min Hee</creatorcontrib><title>The Significance of Targeting Poly (ADP-Ribose) Polymerase-1 in Pancreatic Cancer for Providing a New Therapeutic Paradigm</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Genome-wide studies focusing on elucidating the effects on cancer progression have enabled the consequent identification of a distinct subpopulation of pancreatic cancer cells with unstable genomic characteristics. Based on this background, deleterious changes by poly (adenosine diphosphate (ADP)-ribose) polymerase-1 (PARP)-1 have been concentrated in oncology. One of the critical functions of PARP-1 is the response to DNA damage, which plays a pivotal role in DNA repair in cancers. PARP-1 also has widespread functions that are essential for the survival and growth of cancer cells. It regulates oxidative stress in mitochondria through the regulation of superoxide and oxidation. PARP-1 is in charge of regulating mitosis, which is a crucial role in tumorigenesis and remodels histones and chromatin enzymes related to transcriptional regulation, causing alterations in epigenetic markers and chromatin structure. Given the significance of these processes, it can be understood that these processes in cancer cells are at the frontline of the pathogenetic changes required for cancer cell survival, and these contributions can result in malignant transformation. Therefore, this review addresses the current molecular biological features for understanding the multifactorial function of PARP-1 in pancreatic cancer related to the aforementioned roles, along with the summary of recent approaches with PARP-1 inhibition in clinical studies targeting pancreatic cancer. This understanding could help to embrace the importance of targeting PARP-1 in the treatment of pancreatic cancer, which may present the potential to find out a variety of research topics that can be both challenged clinically and non-clinically.</description><subject>Adenosine</subject><subject>Adenosine diphosphate</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Chromatin</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>DNA Repair</subject><subject>Drug resistance</subject><subject>Enzymes</subject><subject>Epigenetics</subject><subject>Gene expression</subject><subject>Gene regulation</subject><subject>Genomes</subject><subject>Histones</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Kinases</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Mitochondria</subject><subject>Mitosis</subject><subject>Mutation</subject><subject>Oxidation</subject><subject>Oxidative Stress</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pathogenesis</subject><subject>Physiology</subject><subject>Poly (ADP-Ribose) Polymerase-1 - antagonists & inhibitors</subject><subject>Poly (ADP-Ribose) Polymerase-1 - metabolism</subject><subject>Poly(ADP-ribose) polymerase</subject><subject>Proteins</subject><subject>Review</subject><subject>Ribose</subject><subject>Survival</subject><subject>Transcription</subject><subject>Transcription factors</subject><subject>Transcription, Genetic</subject><subject>Tumorigenesis</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkU1v1DAQhi0Eoh9w44wscWklArYnTuwLUrV8ShVEsJwtx5mkXiXxYidF5deT0FItnGzZzzwzo5eQZ5y9AtDstd8NSQhWgmT6ATnmuRAZY0X58OB-RE5S2jEmQEj9mBwBKCaFhmPya3uF9JvvRt96Z0eHNLR0a2OHkx87WoX-hp5dvK2yr74OCc__vAwYbcKMUz_SaimKaCfv6Gatj7QNkVYxXPtmNVj6GX_SpUu0e5xXrLLRNr4bnpBHre0TPr07T8n39--2m4_Z5ZcPnzYXl5nLuZiyXDStZk5LgblkCguoZVPIRtWY56C4AGvrMpdCcAeuaREcFIzrwikLVik4JW9uvfu5HrBxOE7R9mYf_WDjjQnWm39_Rn9lunBtFINSl3wRnN0JYvgxY5rM4JPDvrcjhjkZsYwli0KpYkFf_IfuwhzHZb2FylVZagar8OUt5WJIKWJ7PwxnZg3VHIa64M8PF7iH_6YIvwFgQJ04</recordid><startdate>20210329</startdate><enddate>20210329</enddate><creator>Jeong, Keun-Yeong</creator><creator>Park, Min Hee</creator><general>MDPI AG</general><general>MDPI</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20210329</creationdate><title>The Significance of Targeting Poly (ADP-Ribose) Polymerase-1 in Pancreatic Cancer for Providing a New Therapeutic Paradigm</title><author>Jeong, Keun-Yeong ; Park, Min Hee</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-42df90c952e4508e63b5d65d8be4438123aab745221c3cdfe3c360196c8a3a883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adenosine</topic><topic>Adenosine diphosphate</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Chromatin</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>DNA Repair</topic><topic>Drug resistance</topic><topic>Enzymes</topic><topic>Epigenetics</topic><topic>Gene expression</topic><topic>Gene regulation</topic><topic>Genomes</topic><topic>Histones</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Kinases</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Mitochondria</topic><topic>Mitosis</topic><topic>Mutation</topic><topic>Oxidation</topic><topic>Oxidative Stress</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pathogenesis</topic><topic>Physiology</topic><topic>Poly (ADP-Ribose) Polymerase-1 - antagonists & inhibitors</topic><topic>Poly (ADP-Ribose) Polymerase-1 - metabolism</topic><topic>Poly(ADP-ribose) polymerase</topic><topic>Proteins</topic><topic>Review</topic><topic>Ribose</topic><topic>Survival</topic><topic>Transcription</topic><topic>Transcription factors</topic><topic>Transcription, Genetic</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jeong, Keun-Yeong</creatorcontrib><creatorcontrib>Park, Min Hee</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jeong, Keun-Yeong</au><au>Park, Min Hee</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Significance of Targeting Poly (ADP-Ribose) Polymerase-1 in Pancreatic Cancer for Providing a New Therapeutic Paradigm</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2021-03-29</date><risdate>2021</risdate><volume>22</volume><issue>7</issue><spage>3509</spage><pages>3509-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Genome-wide studies focusing on elucidating the effects on cancer progression have enabled the consequent identification of a distinct subpopulation of pancreatic cancer cells with unstable genomic characteristics. Based on this background, deleterious changes by poly (adenosine diphosphate (ADP)-ribose) polymerase-1 (PARP)-1 have been concentrated in oncology. One of the critical functions of PARP-1 is the response to DNA damage, which plays a pivotal role in DNA repair in cancers. PARP-1 also has widespread functions that are essential for the survival and growth of cancer cells. It regulates oxidative stress in mitochondria through the regulation of superoxide and oxidation. PARP-1 is in charge of regulating mitosis, which is a crucial role in tumorigenesis and remodels histones and chromatin enzymes related to transcriptional regulation, causing alterations in epigenetic markers and chromatin structure. Given the significance of these processes, it can be understood that these processes in cancer cells are at the frontline of the pathogenetic changes required for cancer cell survival, and these contributions can result in malignant transformation. Therefore, this review addresses the current molecular biological features for understanding the multifactorial function of PARP-1 in pancreatic cancer related to the aforementioned roles, along with the summary of recent approaches with PARP-1 inhibition in clinical studies targeting pancreatic cancer. This understanding could help to embrace the importance of targeting PARP-1 in the treatment of pancreatic cancer, which may present the potential to find out a variety of research topics that can be both challenged clinically and non-clinically.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>33805293</pmid><doi>10.3390/ijms22073509</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Adenosine Adenosine diphosphate Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Antioxidants Apoptosis Cancer therapies Cell cycle Chromatin Deoxyribonucleic acid DNA DNA Damage DNA Repair Drug resistance Enzymes Epigenetics Gene expression Gene regulation Genomes Histones Homeostasis Humans Hypoxia Kinases Metabolism Metabolites Mitochondria Mitosis Mutation Oxidation Oxidative Stress Pancreatic cancer Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pathogenesis Physiology Poly (ADP-Ribose) Polymerase-1 - antagonists & inhibitors Poly (ADP-Ribose) Polymerase-1 - metabolism Poly(ADP-ribose) polymerase Proteins Review Ribose Survival Transcription Transcription factors Transcription, Genetic Tumorigenesis |
| title | The Significance of Targeting Poly (ADP-Ribose) Polymerase-1 in Pancreatic Cancer for Providing a New Therapeutic Paradigm |
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