The functional role of peroxiredoxin 3 in reactive oxygen species, apoptosis, and chemoresistance of cancer cells
Purpose The mammalian peroxiredoxin (PRX) family contains six members that provide antioxidant defense in different cell types by removing reactive oxygen species (ROS) through conserved active cysteines. Different from other members, PRX3 is predominantly located in mitochondria, a major apoptosis...
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| Veröffentlicht in: | Journal of Cancer Research & Clinical Oncology 2015-12, Vol.141 (12), p.2071-2077 |
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| container_title | Journal of Cancer Research & Clinical Oncology |
| container_volume | 141 |
| creator | Li, Lianqin Yu, Ai-Qun |
| description | Purpose
The mammalian peroxiredoxin (PRX) family contains six members that provide antioxidant defense in different cell types by removing reactive oxygen species (ROS) through conserved active cysteines. Different from other members, PRX3 is predominantly located in mitochondria, a major apoptosis mediator. The purpose of this review is to summarize the findings on PRX3 concerning its role in ROS removal, apoptosis, and chemoresistance of cancer cells.
Methods
The relevant literature from PubMed and Medline databases is reviewed in this article (1994-2014).
Results
Because of fast growth and relatively low supply of oxygen in cancer cells, ROS production from mitochondria is exaggerated to an extent that overwhelms cellular antioxidant defenses resulting in oxidative stress. As an active responder to oxidative stress, PRX3 is accordingly up-regulated in cancer cells to remove cellular ROS and inhibit apoptosis, which provides a favorable microenvironment for cell proliferation.
Conclusion
Since most of chemotherapy or radiotherapy for cancers is through ROS increase and apoptotic induction, PRX3 might be involved in the chemotherapeutic resistance of cancers. |
| doi_str_mv | 10.1007/s00432-015-1916-3 |
| format | Article |
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The mammalian peroxiredoxin (PRX) family contains six members that provide antioxidant defense in different cell types by removing reactive oxygen species (ROS) through conserved active cysteines. Different from other members, PRX3 is predominantly located in mitochondria, a major apoptosis mediator. The purpose of this review is to summarize the findings on PRX3 concerning its role in ROS removal, apoptosis, and chemoresistance of cancer cells.
Methods
The relevant literature from PubMed and Medline databases is reviewed in this article (1994-2014).
Results
Because of fast growth and relatively low supply of oxygen in cancer cells, ROS production from mitochondria is exaggerated to an extent that overwhelms cellular antioxidant defenses resulting in oxidative stress. As an active responder to oxidative stress, PRX3 is accordingly up-regulated in cancer cells to remove cellular ROS and inhibit apoptosis, which provides a favorable microenvironment for cell proliferation.
Conclusion
Since most of chemotherapy or radiotherapy for cancers is through ROS increase and apoptotic induction, PRX3 might be involved in the chemotherapeutic resistance of cancers.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s00432-015-1916-3</identifier><identifier>PMID: 25875582</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Antioxidants ; Apoptosis ; Cancer ; Cancer Research ; Drug Resistance, Neoplasm ; Hematology ; Humans ; Internal Medicine ; Medicine ; Medicine & Public Health ; Mitochondria ; Neoplasms - drug therapy ; Neoplasms - metabolism ; Neoplasms - pathology ; Oncology ; Oxidative Stress ; Peroxiredoxin III - metabolism ; Reactive Oxygen Species - metabolism ; Review – Cancer Research</subject><ispartof>Journal of Cancer Research & Clinical Oncology, 2015-12, Vol.141 (12), p.2071-2077</ispartof><rights>Springer-Verlag Berlin Heidelberg 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-4fb131243525c6f38134cd41bf6e37d74af41e5474e5fb907a90e896a514143b3</citedby><cites>FETCH-LOGICAL-c442t-4fb131243525c6f38134cd41bf6e37d74af41e5474e5fb907a90e896a514143b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00432-015-1916-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00432-015-1916-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,315,781,785,793,27927,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25875582$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Lianqin</creatorcontrib><creatorcontrib>Yu, Ai-Qun</creatorcontrib><title>The functional role of peroxiredoxin 3 in reactive oxygen species, apoptosis, and chemoresistance of cancer cells</title><title>Journal of Cancer Research & Clinical Oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><addtitle>J Cancer Res Clin Oncol</addtitle><description>Purpose
The mammalian peroxiredoxin (PRX) family contains six members that provide antioxidant defense in different cell types by removing reactive oxygen species (ROS) through conserved active cysteines. Different from other members, PRX3 is predominantly located in mitochondria, a major apoptosis mediator. The purpose of this review is to summarize the findings on PRX3 concerning its role in ROS removal, apoptosis, and chemoresistance of cancer cells.
Methods
The relevant literature from PubMed and Medline databases is reviewed in this article (1994-2014).
Results
Because of fast growth and relatively low supply of oxygen in cancer cells, ROS production from mitochondria is exaggerated to an extent that overwhelms cellular antioxidant defenses resulting in oxidative stress. As an active responder to oxidative stress, PRX3 is accordingly up-regulated in cancer cells to remove cellular ROS and inhibit apoptosis, which provides a favorable microenvironment for cell proliferation.
Conclusion
Since most of chemotherapy or radiotherapy for cancers is through ROS increase and apoptotic induction, PRX3 might be involved in the chemotherapeutic resistance of cancers.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>Drug Resistance, Neoplasm</subject><subject>Hematology</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mitochondria</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Oncology</subject><subject>Oxidative Stress</subject><subject>Peroxiredoxin III - metabolism</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Review – Cancer Research</subject><issn>0171-5216</issn><issn>1432-1335</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kU1P3DAQhi1UxG6BH9BLZakXDg14_BEnxwpBWwmJC5wtxxkvQdk4aycV_Ps67FJVlXoZz3ieeW3NS8gnYJfAmL5KjEnBCwaqgBrKQhyRNSw3IIT6QNYMNBSKQ7kiH1N6ZrlWmp-QFVeVVqria7J7eELq58FNXRhsT2PokQZPR4zhpYvY5jhQQXOIaDP1K7dfXjc40DSi6zB9pXYM4xRSt6RDS90TbkPEXE92cG9qbkkiddj36Ywce9snPD-cp-Tx9ubh-kdxd__95_W3u8JJyadC-gYEcCkUV670ogIhXSuh8SUK3WppvQRUUktUvqmZtjXDqi6tApl30IhTcrHXHWPYzZgms-3S8gM7YJiTAS0Y41xXVUa__IM-hznmdSwUz6J1_UbBnnIxpBTRmzF2WxtfDTCz-GH2fpjsh1n8MCLPfD4oz80W2z8T7wZkgO-BlFvDBuNfT_9X9TfBEpUc</recordid><startdate>20151201</startdate><enddate>20151201</enddate><creator>Li, Lianqin</creator><creator>Yu, Ai-Qun</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</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>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20151201</creationdate><title>The functional role of peroxiredoxin 3 in reactive oxygen species, apoptosis, and chemoresistance of cancer cells</title><author>Li, Lianqin ; Yu, Ai-Qun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-4fb131243525c6f38134cd41bf6e37d74af41e5474e5fb907a90e896a514143b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Cancer</topic><topic>Cancer Research</topic><topic>Drug Resistance, Neoplasm</topic><topic>Hematology</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mitochondria</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Oncology</topic><topic>Oxidative Stress</topic><topic>Peroxiredoxin III - metabolism</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Review – Cancer Research</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Lianqin</creatorcontrib><creatorcontrib>Yu, Ai-Qun</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>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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)</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</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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Research Library (ProQuest)</collection><collection>Research Library (Corporate)</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><jtitle>Journal of Cancer Research & Clinical Oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Lianqin</au><au>Yu, Ai-Qun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The functional role of peroxiredoxin 3 in reactive oxygen species, apoptosis, and chemoresistance of cancer cells</atitle><jtitle>Journal of Cancer Research & Clinical Oncology</jtitle><stitle>J Cancer Res Clin Oncol</stitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2015-12-01</date><risdate>2015</risdate><volume>141</volume><issue>12</issue><spage>2071</spage><epage>2077</epage><pages>2071-2077</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><abstract>Purpose
The mammalian peroxiredoxin (PRX) family contains six members that provide antioxidant defense in different cell types by removing reactive oxygen species (ROS) through conserved active cysteines. Different from other members, PRX3 is predominantly located in mitochondria, a major apoptosis mediator. The purpose of this review is to summarize the findings on PRX3 concerning its role in ROS removal, apoptosis, and chemoresistance of cancer cells.
Methods
The relevant literature from PubMed and Medline databases is reviewed in this article (1994-2014).
Results
Because of fast growth and relatively low supply of oxygen in cancer cells, ROS production from mitochondria is exaggerated to an extent that overwhelms cellular antioxidant defenses resulting in oxidative stress. As an active responder to oxidative stress, PRX3 is accordingly up-regulated in cancer cells to remove cellular ROS and inhibit apoptosis, which provides a favorable microenvironment for cell proliferation.
Conclusion
Since most of chemotherapy or radiotherapy for cancers is through ROS increase and apoptotic induction, PRX3 might be involved in the chemotherapeutic resistance of cancers.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>25875582</pmid><doi>10.1007/s00432-015-1916-3</doi><tpages>7</tpages></addata></record> |
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| identifier | ISSN: 0171-5216 |
| ispartof | Journal of Cancer Research & Clinical Oncology, 2015-12, Vol.141 (12), p.2071-2077 |
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| source | MEDLINE; Springer journals |
| subjects | Animals Antioxidants Apoptosis Cancer Cancer Research Drug Resistance, Neoplasm Hematology Humans Internal Medicine Medicine Medicine & Public Health Mitochondria Neoplasms - drug therapy Neoplasms - metabolism Neoplasms - pathology Oncology Oxidative Stress Peroxiredoxin III - metabolism Reactive Oxygen Species - metabolism Review – Cancer Research |
| title | The functional role of peroxiredoxin 3 in reactive oxygen species, apoptosis, and chemoresistance of cancer cells |
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