The NRF2 transcription factor plays a dual role in colorectal cancer: A systematic review
Colorectal cancer is one of the most common cancers worldwide, and is influenced by the interplay of various factors, including a very strong genetic component. For instance, incorrect mitochondrial biogenesis is correlated with increased risk of developing colorectal cancer. Thus, it is important t...
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| description | Colorectal cancer is one of the most common cancers worldwide, and is influenced by the interplay of various factors, including a very strong genetic component. For instance, incorrect mitochondrial biogenesis is correlated with increased risk of developing colorectal cancer. Thus, it is important to understand the consequences of changes in both the expression and the correct function of the transcription factors that regulate mitochondrial biogenesis, namely NRF2.
The main objective of this paper is to characterise the relationship between NRF2 and colorectal cancer by compiling data from an exhaustive literature search.
Information was obtained by defining specific search terms and searching in several databases. After a strict selection procedure, data were tabulated and the relationships between articles were assessed by measuring heterogeneity and by constructing conceptual maps.
We found a general consensus in the literature that the presence of oxidizing agents as well as the inhibition of the NRF2 repressor Keap1 maintain NRF2 expression at basal levels. This predominantly exerts a cytoprotective effect on cells and decreases risk of colorectal cancer. However, if NRF2 is inhibited, protection against external agents disappears and risk of colorectal cancer increases. Interestingly, colorectal cancer risk is also increased when NRF2 becomes overexpressed. In this case, the increased risk arises from NRF2-induced inflammation and resistance to chemotherapy.
The proper basal function of NRF2 and Keap1 are essential for preventing oncogenic processes in the colon. Consequently, any disruption to the expression of these genes can promote the genesis and progression of colon cancer. |
| doi_str_mv | 10.1371/journal.pone.0177549 |
| format | Article |
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The main objective of this paper is to characterise the relationship between NRF2 and colorectal cancer by compiling data from an exhaustive literature search.
Information was obtained by defining specific search terms and searching in several databases. After a strict selection procedure, data were tabulated and the relationships between articles were assessed by measuring heterogeneity and by constructing conceptual maps.
We found a general consensus in the literature that the presence of oxidizing agents as well as the inhibition of the NRF2 repressor Keap1 maintain NRF2 expression at basal levels. This predominantly exerts a cytoprotective effect on cells and decreases risk of colorectal cancer. However, if NRF2 is inhibited, protection against external agents disappears and risk of colorectal cancer increases. Interestingly, colorectal cancer risk is also increased when NRF2 becomes overexpressed. In this case, the increased risk arises from NRF2-induced inflammation and resistance to chemotherapy.
The proper basal function of NRF2 and Keap1 are essential for preventing oncogenic processes in the colon. Consequently, any disruption to the expression of these genes can promote the genesis and progression of colon cancer.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0177549</identifier><identifier>PMID: 28542357</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>5-Fluorouracil ; Aberration ; Activation ; Adenoma ; Analysis ; Antioxidants ; Apoptosis ; Atmospheric pressure ; Attenuation ; Biochemistry ; Biology and Life Sciences ; Biosynthesis ; Boolean algebra ; c-Met protein ; Cancer ; Carcinogenesis ; Cell death ; Cell fate ; Cell survival ; Chemotherapy ; Chronic lymphocytic leukemia ; Citation management software ; Colitis ; Colon ; Colorectal cancer ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - metabolism ; Correlation ; Differentiation ; Flow charts ; Gene Expression Regulation, Neoplastic ; Genes ; Genetic aspects ; Genomes ; Health risks ; Humans ; Inflammation ; Inhibition ; Intestine ; Libraries ; Lipids ; Medical research ; Medicine and Health Sciences ; Metabolism ; NF-E2-Related Factor 2 - metabolism ; Nuclear reactions ; Nucleic acids ; Oxidative stress ; Oxidizing agents ; Pharmacology ; Proteins ; Radiation therapy ; Rectum ; Research and Analysis Methods ; Risk factors ; Rodents ; Signal transduction ; Stem cells ; Stresses ; Survival ; Transcription factors ; Tumorigenesis ; Tumors</subject><ispartof>PloS one, 2017-05, Vol.12 (5), p.e0177549</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Gonzalez-Donquiles et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Gonzalez-Donquiles et al 2017 Gonzalez-Donquiles et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-49334c2e79de7f201d35d3124d29f2c79b903bc1fea262fa45cbd4e6fcdc06343</citedby><cites>FETCH-LOGICAL-c758t-49334c2e79de7f201d35d3124d29f2c79b903bc1fea262fa45cbd4e6fcdc06343</cites><orcidid>0000-0001-6212-1797</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5436741/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5436741/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28542357$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gonzalez-Donquiles, C</creatorcontrib><creatorcontrib>Alonso-Molero, J</creatorcontrib><creatorcontrib>Fernandez-Villa, T</creatorcontrib><creatorcontrib>Vilorio-Marqués, L</creatorcontrib><creatorcontrib>Molina, A J</creatorcontrib><creatorcontrib>Martín, V</creatorcontrib><title>The NRF2 transcription factor plays a dual role in colorectal cancer: A systematic review</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Colorectal cancer is one of the most common cancers worldwide, and is influenced by the interplay of various factors, including a very strong genetic component. For instance, incorrect mitochondrial biogenesis is correlated with increased risk of developing colorectal cancer. Thus, it is important to understand the consequences of changes in both the expression and the correct function of the transcription factors that regulate mitochondrial biogenesis, namely NRF2.
The main objective of this paper is to characterise the relationship between NRF2 and colorectal cancer by compiling data from an exhaustive literature search.
Information was obtained by defining specific search terms and searching in several databases. After a strict selection procedure, data were tabulated and the relationships between articles were assessed by measuring heterogeneity and by constructing conceptual maps.
We found a general consensus in the literature that the presence of oxidizing agents as well as the inhibition of the NRF2 repressor Keap1 maintain NRF2 expression at basal levels. This predominantly exerts a cytoprotective effect on cells and decreases risk of colorectal cancer. However, if NRF2 is inhibited, protection against external agents disappears and risk of colorectal cancer increases. Interestingly, colorectal cancer risk is also increased when NRF2 becomes overexpressed. In this case, the increased risk arises from NRF2-induced inflammation and resistance to chemotherapy.
The proper basal function of NRF2 and Keap1 are essential for preventing oncogenic processes in the colon. Consequently, any disruption to the expression of these genes can promote the genesis and progression of colon cancer.</description><subject>5-Fluorouracil</subject><subject>Aberration</subject><subject>Activation</subject><subject>Adenoma</subject><subject>Analysis</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Atmospheric pressure</subject><subject>Attenuation</subject><subject>Biochemistry</subject><subject>Biology and Life Sciences</subject><subject>Biosynthesis</subject><subject>Boolean algebra</subject><subject>c-Met protein</subject><subject>Cancer</subject><subject>Carcinogenesis</subject><subject>Cell death</subject><subject>Cell fate</subject><subject>Cell survival</subject><subject>Chemotherapy</subject><subject>Chronic lymphocytic leukemia</subject><subject>Citation management software</subject><subject>Colitis</subject><subject>Colon</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - 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NRF2 transcription factor plays a dual role in colorectal cancer: A systematic review</title><author>Gonzalez-Donquiles, C ; Alonso-Molero, J ; Fernandez-Villa, T ; Vilorio-Marqués, L ; Molina, A J ; Martín, V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-49334c2e79de7f201d35d3124d29f2c79b903bc1fea262fa45cbd4e6fcdc06343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>5-Fluorouracil</topic><topic>Aberration</topic><topic>Activation</topic><topic>Adenoma</topic><topic>Analysis</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Atmospheric pressure</topic><topic>Attenuation</topic><topic>Biochemistry</topic><topic>Biology and Life Sciences</topic><topic>Biosynthesis</topic><topic>Boolean algebra</topic><topic>c-Met protein</topic><topic>Cancer</topic><topic>Carcinogenesis</topic><topic>Cell death</topic><topic>Cell fate</topic><topic>Cell 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V</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The NRF2 transcription factor plays a dual role in colorectal cancer: A systematic review</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-05-18</date><risdate>2017</risdate><volume>12</volume><issue>5</issue><spage>e0177549</spage><pages>e0177549-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Colorectal cancer is one of the most common cancers worldwide, and is influenced by the interplay of various factors, including a very strong genetic component. For instance, incorrect mitochondrial biogenesis is correlated with increased risk of developing colorectal cancer. Thus, it is important to understand the consequences of changes in both the expression and the correct function of the transcription factors that regulate mitochondrial biogenesis, namely NRF2.
The main objective of this paper is to characterise the relationship between NRF2 and colorectal cancer by compiling data from an exhaustive literature search.
Information was obtained by defining specific search terms and searching in several databases. After a strict selection procedure, data were tabulated and the relationships between articles were assessed by measuring heterogeneity and by constructing conceptual maps.
We found a general consensus in the literature that the presence of oxidizing agents as well as the inhibition of the NRF2 repressor Keap1 maintain NRF2 expression at basal levels. This predominantly exerts a cytoprotective effect on cells and decreases risk of colorectal cancer. However, if NRF2 is inhibited, protection against external agents disappears and risk of colorectal cancer increases. Interestingly, colorectal cancer risk is also increased when NRF2 becomes overexpressed. In this case, the increased risk arises from NRF2-induced inflammation and resistance to chemotherapy.
The proper basal function of NRF2 and Keap1 are essential for preventing oncogenic processes in the colon. Consequently, any disruption to the expression of these genes can promote the genesis and progression of colon cancer.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28542357</pmid><doi>10.1371/journal.pone.0177549</doi><tpages>e0177549</tpages><orcidid>https://orcid.org/0000-0001-6212-1797</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2017-05, Vol.12 (5), p.e0177549 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1900218066 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 5-Fluorouracil Aberration Activation Adenoma Analysis Antioxidants Apoptosis Atmospheric pressure Attenuation Biochemistry Biology and Life Sciences Biosynthesis Boolean algebra c-Met protein Cancer Carcinogenesis Cell death Cell fate Cell survival Chemotherapy Chronic lymphocytic leukemia Citation management software Colitis Colon Colorectal cancer Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Correlation Differentiation Flow charts Gene Expression Regulation, Neoplastic Genes Genetic aspects Genomes Health risks Humans Inflammation Inhibition Intestine Libraries Lipids Medical research Medicine and Health Sciences Metabolism NF-E2-Related Factor 2 - metabolism Nuclear reactions Nucleic acids Oxidative stress Oxidizing agents Pharmacology Proteins Radiation therapy Rectum Research and Analysis Methods Risk factors Rodents Signal transduction Stem cells Stresses Survival Transcription factors Tumorigenesis Tumors |
| title | The NRF2 transcription factor plays a dual role in colorectal cancer: A systematic review |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-01T07%3A07%3A40IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20NRF2%20transcription%20factor%20plays%20a%20dual%20role%20in%20colorectal%20cancer:%20A%20systematic%20review&rft.jtitle=PloS%20one&rft.au=Gonzalez-Donquiles,%20C&rft.date=2017-05-18&rft.volume=12&rft.issue=5&rft.spage=e0177549&rft.pages=e0177549-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0177549&rft_dat=%3Cgale_plos_%3EA491954284%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1900218066&rft_id=info:pmid/28542357&rft_galeid=A491954284&rft_doaj_id=oai_doaj_org_article_97092d745240474f8088c4fce2c064ad&rfr_iscdi=true |