Reactive oxygen species in colorectal cancer: The therapeutic impact and its potential roles in tumor progression via perturbation of cellular and physiological dysregulated pathways
Reactive oxygen species (ROS) are produced by mitochondria during metabolism. In physiological states, the production of ROS and their elimination by antioxidants are kept in balance. However, in pathological states, elevated levels of ROS interact with susceptible cellular target compounds includin...
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Veröffentlicht in: | Journal of cellular physiology 2019-07, Vol.234 (7), p.10072-10079 |
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description | Reactive oxygen species (ROS) are produced by mitochondria during metabolism. In physiological states, the production of ROS and their elimination by antioxidants are kept in balance. However, in pathological states, elevated levels of ROS interact with susceptible cellular target compounds including lipids, proteins, and DNA and deregulate oncogenic signaling pathways that are involved in colorectal cancer (CRC) carcinogenesis. Although antioxidant compounds have been successfully used in the treatment of CRC as prevention approaches, they have also been shown in some cases to promote disease progression. In this review, we focus on the role of ROS in gastrointestinal homeostasis, CRC progression, diagnosis, and therapy with particular emphasis on ROS‐stimulated pathways.
The role of redox‐sensitive signaling pathways in colorectal cancer progression. |
doi_str_mv | 10.1002/jcp.27881 |
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The role of redox‐sensitive signaling pathways in colorectal cancer progression.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.27881</identifier><identifier>PMID: 30515827</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Animals ; Antioxidants ; Cancer ; Carcinogenesis ; Carcinogenesis - metabolism ; Carcinogenesis - pathology ; Carcinogens ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Deoxyribonucleic acid ; Deregulation ; Disease Progression ; DNA ; Homeostasis ; Humans ; Lipids ; Metabolism ; Mitochondria ; Oxidation-Reduction ; Oxidative Stress - physiology ; Perturbation ; Physiology ; progression ; Proteins ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Signal Transduction - physiology</subject><ispartof>Journal of cellular physiology, 2019-07, Vol.234 (7), p.10072-10079</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><rights>2019 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3531-cf6931bb2397a9014b1562739bd483d32af95c78b1ebbe1e9003e29eca0c86f13</citedby><cites>FETCH-LOGICAL-c3531-cf6931bb2397a9014b1562739bd483d32af95c78b1ebbe1e9003e29eca0c86f13</cites><orcidid>0000-0003-1024-3906 ; 0000-0002-7979-5699 ; 0000-0003-0773-0906 ; 0000-0002-4968-0962</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.27881$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.27881$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30515827$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moradi‐Marjaneh, Reyhaneh</creatorcontrib><creatorcontrib>Hassanian, Seyed Mahdi</creatorcontrib><creatorcontrib>Mehramiz, Mehraneh</creatorcontrib><creatorcontrib>Rezayi, Majid</creatorcontrib><creatorcontrib>Ferns, Gordon A.</creatorcontrib><creatorcontrib>Khazaei, Majid</creatorcontrib><creatorcontrib>Avan, Amir</creatorcontrib><title>Reactive oxygen species in colorectal cancer: The therapeutic impact and its potential roles in tumor progression via perturbation of cellular and physiological dysregulated pathways</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>Reactive oxygen species (ROS) are produced by mitochondria during metabolism. In physiological states, the production of ROS and their elimination by antioxidants are kept in balance. However, in pathological states, elevated levels of ROS interact with susceptible cellular target compounds including lipids, proteins, and DNA and deregulate oncogenic signaling pathways that are involved in colorectal cancer (CRC) carcinogenesis. Although antioxidant compounds have been successfully used in the treatment of CRC as prevention approaches, they have also been shown in some cases to promote disease progression. In this review, we focus on the role of ROS in gastrointestinal homeostasis, CRC progression, diagnosis, and therapy with particular emphasis on ROS‐stimulated pathways.
The role of redox‐sensitive signaling pathways in colorectal cancer progression.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Cancer</subject><subject>Carcinogenesis</subject><subject>Carcinogenesis - metabolism</subject><subject>Carcinogenesis - pathology</subject><subject>Carcinogens</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Deoxyribonucleic acid</subject><subject>Deregulation</subject><subject>Disease Progression</subject><subject>DNA</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Lipids</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Oxidation-Reduction</subject><subject>Oxidative Stress - physiology</subject><subject>Perturbation</subject><subject>Physiology</subject><subject>progression</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction - physiology</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1O3DAYRS0EgmHooi9QWWLVRcA_k0ncXTUqpRUSCNF1ZDtfZjzyxMZ2gLxYn69mAt2xsuR7vuOfi9BnSi4oIexyq_0Fq-qaHqAZJaIqFsuSHaJZzmghygU9QacxbgkhQnB-jE44KWlZs2qG_t6D1Mk8AXYv4xp6HD1oAxGbHmtnXQCdpMVa9hrCN_ywAZw2EKSHIRmNzc7ncSz7FpsUsXcJ-mTyQHB2kqRh5wL2wa0DxGhcj5-MxB5CGoKS6XXDdViDtYOVYW_ymzGD1q2NzqZ2jAHWOUyQI5k2z3KMZ-iokzbCp7d1jv5c_XhYXRc3tz9_rb7fFJqXnBa6WwpOlWJcVFIQulC0XLKKC9Uuat5yJjtR6qpWFJQCCoIQDkyAlkTXy47yOTqfvPkBjwPE1GzdEPp8ZMNo_kvCBWOZ-jpROriYb9s1PpidDGNDSfPaUJMbavYNZfbLm3FQO2j_k--VZOByAp6NhfFjU_N7dTcp_wGIN5-j</recordid><startdate>201907</startdate><enddate>201907</enddate><creator>Moradi‐Marjaneh, Reyhaneh</creator><creator>Hassanian, Seyed Mahdi</creator><creator>Mehramiz, Mehraneh</creator><creator>Rezayi, Majid</creator><creator>Ferns, Gordon A.</creator><creator>Khazaei, Majid</creator><creator>Avan, Amir</creator><general>Wiley Subscription Services, Inc</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>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><orcidid>https://orcid.org/0000-0003-1024-3906</orcidid><orcidid>https://orcid.org/0000-0002-7979-5699</orcidid><orcidid>https://orcid.org/0000-0003-0773-0906</orcidid><orcidid>https://orcid.org/0000-0002-4968-0962</orcidid></search><sort><creationdate>201907</creationdate><title>Reactive oxygen species in colorectal cancer: The therapeutic impact and its potential roles in tumor progression via perturbation of cellular and physiological dysregulated pathways</title><author>Moradi‐Marjaneh, Reyhaneh ; Hassanian, Seyed Mahdi ; Mehramiz, Mehraneh ; Rezayi, Majid ; Ferns, Gordon A. ; Khazaei, Majid ; Avan, Amir</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3531-cf6931bb2397a9014b1562739bd483d32af95c78b1ebbe1e9003e29eca0c86f13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Antioxidants</topic><topic>Cancer</topic><topic>Carcinogenesis</topic><topic>Carcinogenesis - metabolism</topic><topic>Carcinogenesis - pathology</topic><topic>Carcinogens</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Deoxyribonucleic acid</topic><topic>Deregulation</topic><topic>Disease Progression</topic><topic>DNA</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Lipids</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Oxidation-Reduction</topic><topic>Oxidative Stress - physiology</topic><topic>Perturbation</topic><topic>Physiology</topic><topic>progression</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal Transduction - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moradi‐Marjaneh, Reyhaneh</creatorcontrib><creatorcontrib>Hassanian, Seyed Mahdi</creatorcontrib><creatorcontrib>Mehramiz, Mehraneh</creatorcontrib><creatorcontrib>Rezayi, Majid</creatorcontrib><creatorcontrib>Ferns, Gordon A.</creatorcontrib><creatorcontrib>Khazaei, Majid</creatorcontrib><creatorcontrib>Avan, Amir</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moradi‐Marjaneh, Reyhaneh</au><au>Hassanian, Seyed Mahdi</au><au>Mehramiz, Mehraneh</au><au>Rezayi, Majid</au><au>Ferns, Gordon A.</au><au>Khazaei, Majid</au><au>Avan, Amir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reactive oxygen species in colorectal cancer: The therapeutic impact and its potential roles in tumor progression via perturbation of cellular and physiological dysregulated pathways</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2019-07</date><risdate>2019</risdate><volume>234</volume><issue>7</issue><spage>10072</spage><epage>10079</epage><pages>10072-10079</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>Reactive oxygen species (ROS) are produced by mitochondria during metabolism. In physiological states, the production of ROS and their elimination by antioxidants are kept in balance. However, in pathological states, elevated levels of ROS interact with susceptible cellular target compounds including lipids, proteins, and DNA and deregulate oncogenic signaling pathways that are involved in colorectal cancer (CRC) carcinogenesis. Although antioxidant compounds have been successfully used in the treatment of CRC as prevention approaches, they have also been shown in some cases to promote disease progression. In this review, we focus on the role of ROS in gastrointestinal homeostasis, CRC progression, diagnosis, and therapy with particular emphasis on ROS‐stimulated pathways.
The role of redox‐sensitive signaling pathways in colorectal cancer progression.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30515827</pmid><doi>10.1002/jcp.27881</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-1024-3906</orcidid><orcidid>https://orcid.org/0000-0002-7979-5699</orcidid><orcidid>https://orcid.org/0000-0003-0773-0906</orcidid><orcidid>https://orcid.org/0000-0002-4968-0962</orcidid></addata></record> |
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subjects | Animals Antioxidants Cancer Carcinogenesis Carcinogenesis - metabolism Carcinogenesis - pathology Carcinogens Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Deoxyribonucleic acid Deregulation Disease Progression DNA Homeostasis Humans Lipids Metabolism Mitochondria Oxidation-Reduction Oxidative Stress - physiology Perturbation Physiology progression Proteins Reactive oxygen species Reactive Oxygen Species - metabolism Signal Transduction - physiology |
title | Reactive oxygen species in colorectal cancer: The therapeutic impact and its potential roles in tumor progression via perturbation of cellular and physiological dysregulated pathways |
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