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Metabolic Rate and Oxidative Stress as a Risk Factors in the Development of Colorectal Cancer
There is growing evidence that the body's energy expenditures constitute a significant risk factor for the development of most deadly diseases, including cancer. Our aim was to investigate the impact of basal metabolic rate (BMR) on the growth and progression of colorectal cancer (CRC). To do s...
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Published in: | International journal of molecular sciences 2024-10, Vol.25 (19), p.10713 |
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creator | Sawicka, Diana Maciak, Sebastian Sadowska, Anna Sokołowska, Emilia Gohal, Sylwia Guzińska-Ustymowicz, Katarzyna Niemirowicz-Laskowska, Katarzyna Car, Halina |
description | There is growing evidence that the body's energy expenditures constitute a significant risk factor for the development of most deadly diseases, including cancer. Our aim was to investigate the impact of basal metabolic rate (BMR) on the growth and progression of colorectal cancer (CRC). To do so, we used a unique model consisting of three lines of laboratory mice (
) artificially selected for high (HBMR) and low (LBMR) basal metabolic rate and randomly bred individuals (non-selected, NSBMR). The experimental individuals were implanted with human colorectal cancer cells DLD-1. The variation in BMR between the lines allowed for testing the impact of whole-body metabolism on oxidative and antioxidant parameters in the liver throughout the cancerogenesis process. We investigated the dependence between metabolic values, reactive oxygen species (ROS) levels, and Kelch-like ECH-associated protein 1-based E3 ligase complexes (
) gene activity in these animals. We found that the HBMR strain had a higher concentration of oxidative enzymes compared to the LBMR and NSBMR. Furthermore, the growth rate of CRC tumors was associated with alterations in the levels of oxidative stress enzymes and
expression in animals with a high metabolic rate. Our results indicate that a faster growth and development of CRC line DLD-1 is associated with enzymatic redox imbalance in animals with a high BMR. |
doi_str_mv | 10.3390/ijms251910713 |
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) artificially selected for high (HBMR) and low (LBMR) basal metabolic rate and randomly bred individuals (non-selected, NSBMR). The experimental individuals were implanted with human colorectal cancer cells DLD-1. The variation in BMR between the lines allowed for testing the impact of whole-body metabolism on oxidative and antioxidant parameters in the liver throughout the cancerogenesis process. We investigated the dependence between metabolic values, reactive oxygen species (ROS) levels, and Kelch-like ECH-associated protein 1-based E3 ligase complexes (
) gene activity in these animals. We found that the HBMR strain had a higher concentration of oxidative enzymes compared to the LBMR and NSBMR. Furthermore, the growth rate of CRC tumors was associated with alterations in the levels of oxidative stress enzymes and
expression in animals with a high metabolic rate. Our results indicate that a faster growth and development of CRC line DLD-1 is associated with enzymatic redox imbalance in animals with a high BMR.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms251910713</identifier><identifier>PMID: 39409042</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Animals ; Antioxidants ; Basal Metabolism ; Cancer ; Cell Line, Tumor ; Colorectal cancer ; Colorectal Neoplasms - etiology ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Complications and side effects ; Development and progression ; DNA methylation ; Energy ; Enzymes ; Free radicals ; Health aspects ; Homeostasis ; Humans ; Kelch-Like ECH-Associated Protein 1 - metabolism ; Male ; Metabolism ; Mice ; Mitochondrial DNA ; Oncology, Experimental ; Oxidative Stress ; Physiology ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Risk Factors ; Tumors</subject><ispartof>International journal of molecular sciences, 2024-10, Vol.25 (19), p.10713</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 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 (https://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>2024 by the authors. 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c369t-40bc2de3500e1b7de6a80bc9ce929230d562fbe48f98f86d03eb30ee0badb9b93</cites><orcidid>0000-0002-6804-3459 ; 0000-0002-4926-3405 ; 0000-0002-8695-5304 ; 0000-0001-5652-8224 ; 0000-0002-5478-8732</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/3116670877/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/3116670877?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25731,27901,27902,36989,36990,44566,53766,53768,74869</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39409042$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sawicka, Diana</creatorcontrib><creatorcontrib>Maciak, Sebastian</creatorcontrib><creatorcontrib>Sadowska, Anna</creatorcontrib><creatorcontrib>Sokołowska, Emilia</creatorcontrib><creatorcontrib>Gohal, Sylwia</creatorcontrib><creatorcontrib>Guzińska-Ustymowicz, Katarzyna</creatorcontrib><creatorcontrib>Niemirowicz-Laskowska, Katarzyna</creatorcontrib><creatorcontrib>Car, Halina</creatorcontrib><title>Metabolic Rate and Oxidative Stress as a Risk Factors in the Development of Colorectal Cancer</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>There is growing evidence that the body's energy expenditures constitute a significant risk factor for the development of most deadly diseases, including cancer. Our aim was to investigate the impact of basal metabolic rate (BMR) on the growth and progression of colorectal cancer (CRC). To do so, we used a unique model consisting of three lines of laboratory mice (
) artificially selected for high (HBMR) and low (LBMR) basal metabolic rate and randomly bred individuals (non-selected, NSBMR). The experimental individuals were implanted with human colorectal cancer cells DLD-1. The variation in BMR between the lines allowed for testing the impact of whole-body metabolism on oxidative and antioxidant parameters in the liver throughout the cancerogenesis process. We investigated the dependence between metabolic values, reactive oxygen species (ROS) levels, and Kelch-like ECH-associated protein 1-based E3 ligase complexes (
) gene activity in these animals. We found that the HBMR strain had a higher concentration of oxidative enzymes compared to the LBMR and NSBMR. Furthermore, the growth rate of CRC tumors was associated with alterations in the levels of oxidative stress enzymes and
expression in animals with a high metabolic rate. Our results indicate that a faster growth and development of CRC line DLD-1 is associated with enzymatic redox imbalance in animals with a high BMR.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Basal Metabolism</subject><subject>Cancer</subject><subject>Cell Line, Tumor</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - etiology</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Complications and side effects</subject><subject>Development and progression</subject><subject>DNA methylation</subject><subject>Energy</subject><subject>Enzymes</subject><subject>Free radicals</subject><subject>Health aspects</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Kelch-Like ECH-Associated Protein 1 - metabolism</subject><subject>Male</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mitochondrial DNA</subject><subject>Oncology, Experimental</subject><subject>Oxidative Stress</subject><subject>Physiology</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Risk Factors</subject><subject>Tumors</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNptkt9rFDEQxxdR7A999FUCvvRl6yTZTTZPUs5WhZZC1UcJ2exsm3M3OZPcof99c7TWXpEEEiaf-c5M-FbVGwrHnCt475ZzYi1VFCTlz6p92jBWAwj5_NF9rzpIaQnAOGvVy2qPqwYUNGy_-nGB2fRhcpZcmYzE-IFc_naDyW6D5GuOmBIxZZMrl36SM2NziIk4T_INko-4wSmsZvSZhJEswhQi2mwmsjDeYnxVvRjNlPD1_XlYfT87_bb4XJ9ffvqyODmvLRcq1w30lg3IWwCkvRxQmK6ElEXFFOMwtIKNPTbdqLqxEwNw7DkgQm-GXvWKH1Yf7nRX637GwZZ-opn0KrrZxD86GKd3X7y70ddhoyltpGhkWxSO7hVi-LXGlPXsksVpMh7DOmlOqQTZlg4L-u4Jugzr6Mt8W0oICZ2U_6hrM6F2fgylsN2K6pOOMlEKS1Go4_9QZQ04Oxs8jq7EdxLquwQbQ0oRx4chKeitIfSOIQr_9vHPPNB_HcBvAVoLsHM</recordid><startdate>20241005</startdate><enddate>20241005</enddate><creator>Sawicka, Diana</creator><creator>Maciak, Sebastian</creator><creator>Sadowska, Anna</creator><creator>Sokołowska, Emilia</creator><creator>Gohal, Sylwia</creator><creator>Guzińska-Ustymowicz, Katarzyna</creator><creator>Niemirowicz-Laskowska, Katarzyna</creator><creator>Car, Halina</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><orcidid>https://orcid.org/0000-0002-6804-3459</orcidid><orcidid>https://orcid.org/0000-0002-4926-3405</orcidid><orcidid>https://orcid.org/0000-0002-8695-5304</orcidid><orcidid>https://orcid.org/0000-0001-5652-8224</orcidid><orcidid>https://orcid.org/0000-0002-5478-8732</orcidid></search><sort><creationdate>20241005</creationdate><title>Metabolic Rate and Oxidative Stress as a Risk Factors in the Development of Colorectal Cancer</title><author>Sawicka, Diana ; Maciak, Sebastian ; Sadowska, Anna ; Sokołowska, Emilia ; Gohal, Sylwia ; Guzińska-Ustymowicz, Katarzyna ; Niemirowicz-Laskowska, Katarzyna ; Car, Halina</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c369t-40bc2de3500e1b7de6a80bc9ce929230d562fbe48f98f86d03eb30ee0badb9b93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Antioxidants</topic><topic>Basal Metabolism</topic><topic>Cancer</topic><topic>Cell Line, Tumor</topic><topic>Colorectal cancer</topic><topic>Colorectal Neoplasms - etiology</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Complications and side effects</topic><topic>Development and progression</topic><topic>DNA methylation</topic><topic>Energy</topic><topic>Enzymes</topic><topic>Free radicals</topic><topic>Health aspects</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Kelch-Like ECH-Associated Protein 1 - metabolism</topic><topic>Male</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mitochondrial DNA</topic><topic>Oncology, Experimental</topic><topic>Oxidative Stress</topic><topic>Physiology</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Risk Factors</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sawicka, Diana</creatorcontrib><creatorcontrib>Maciak, Sebastian</creatorcontrib><creatorcontrib>Sadowska, Anna</creatorcontrib><creatorcontrib>Sokołowska, Emilia</creatorcontrib><creatorcontrib>Gohal, Sylwia</creatorcontrib><creatorcontrib>Guzińska-Ustymowicz, Katarzyna</creatorcontrib><creatorcontrib>Niemirowicz-Laskowska, Katarzyna</creatorcontrib><creatorcontrib>Car, Halina</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</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>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>Sawicka, Diana</au><au>Maciak, Sebastian</au><au>Sadowska, Anna</au><au>Sokołowska, Emilia</au><au>Gohal, Sylwia</au><au>Guzińska-Ustymowicz, Katarzyna</au><au>Niemirowicz-Laskowska, Katarzyna</au><au>Car, Halina</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metabolic Rate and Oxidative Stress as a Risk Factors in the Development of Colorectal Cancer</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2024-10-05</date><risdate>2024</risdate><volume>25</volume><issue>19</issue><spage>10713</spage><pages>10713-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>There is growing evidence that the body's energy expenditures constitute a significant risk factor for the development of most deadly diseases, including cancer. Our aim was to investigate the impact of basal metabolic rate (BMR) on the growth and progression of colorectal cancer (CRC). To do so, we used a unique model consisting of three lines of laboratory mice (
) artificially selected for high (HBMR) and low (LBMR) basal metabolic rate and randomly bred individuals (non-selected, NSBMR). The experimental individuals were implanted with human colorectal cancer cells DLD-1. The variation in BMR between the lines allowed for testing the impact of whole-body metabolism on oxidative and antioxidant parameters in the liver throughout the cancerogenesis process. We investigated the dependence between metabolic values, reactive oxygen species (ROS) levels, and Kelch-like ECH-associated protein 1-based E3 ligase complexes (
) gene activity in these animals. We found that the HBMR strain had a higher concentration of oxidative enzymes compared to the LBMR and NSBMR. Furthermore, the growth rate of CRC tumors was associated with alterations in the levels of oxidative stress enzymes and
expression in animals with a high metabolic rate. Our results indicate that a faster growth and development of CRC line DLD-1 is associated with enzymatic redox imbalance in animals with a high BMR.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>39409042</pmid><doi>10.3390/ijms251910713</doi><orcidid>https://orcid.org/0000-0002-6804-3459</orcidid><orcidid>https://orcid.org/0000-0002-4926-3405</orcidid><orcidid>https://orcid.org/0000-0002-8695-5304</orcidid><orcidid>https://orcid.org/0000-0001-5652-8224</orcidid><orcidid>https://orcid.org/0000-0002-5478-8732</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animals Antioxidants Basal Metabolism Cancer Cell Line, Tumor Colorectal cancer Colorectal Neoplasms - etiology Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Complications and side effects Development and progression DNA methylation Energy Enzymes Free radicals Health aspects Homeostasis Humans Kelch-Like ECH-Associated Protein 1 - metabolism Male Metabolism Mice Mitochondrial DNA Oncology, Experimental Oxidative Stress Physiology Reactive oxygen species Reactive Oxygen Species - metabolism Risk Factors Tumors |
title | Metabolic Rate and Oxidative Stress as a Risk Factors in the Development of Colorectal Cancer |
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