Chemoprevention by aspirin against inflammation-related colorectal cancer in mice
Inflammation is a primary risk factor for cancer. Epidemiological studies previously demonstrated that aspirin decreased the incidence of cancer and specifically reduced the risk of colorectal cancer. However, the number of animal studies that have confirmed the efficacy of aspirin remains limited....
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| Veröffentlicht in: | Journal of Clinical Biochemistry and Nutrition 2021, Vol.69(3), pp.265-271 |
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| creator | Ohnishi, Shiho Hiramoto, Keiichi Ma, Ning Kawanishi, Shosuke |
| description | Inflammation is a primary risk factor for cancer. Epidemiological studies previously demonstrated that aspirin decreased the incidence of cancer and specifically reduced the risk of colorectal cancer. However, the number of animal studies that have confirmed the efficacy of aspirin remains limited. Therefore, the purpose of the present study was to investigate the mechanisms by which aspirin prevents colorectal cancer in mice. ICR mice were treated with azoxymethane and the ulcerative colitis inducer, dextran sodium sulfate, to induce colorectal tumors. Aspirin was orally administered three times per week for 12 weeks. Aspirin significantly reduced the number and size of colorectal tumors. Aspirin also significantly decreased tumor necrosis factor alpha and reactive oxygen species (ROS) levels in the plasma. Immunohistochemical analyses and western blots showed that cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), and the active form of Yes-associated protein 1 (YAP1), and cytosolic high mobility group box 1 (HMGB1) were strongly expressed at colorectal tumor sites and clearly suppressed by aspirin. An indicator of inflammation-related DNA damage, 8-nitroguanine, also accumulated in the colorectal tissues and was suppressed by aspirin. The present results suggest that the ingestion of aspirin suppressed carcinogenesis caused by inflammation through decreases in COX2 and ROS levels, resulting in reductions in DNA damage and oncogenic YAP1. |
| doi_str_mv | 10.3164/jcbn.20-189 |
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Epidemiological studies previously demonstrated that aspirin decreased the incidence of cancer and specifically reduced the risk of colorectal cancer. However, the number of animal studies that have confirmed the efficacy of aspirin remains limited. Therefore, the purpose of the present study was to investigate the mechanisms by which aspirin prevents colorectal cancer in mice. ICR mice were treated with azoxymethane and the ulcerative colitis inducer, dextran sodium sulfate, to induce colorectal tumors. Aspirin was orally administered three times per week for 12 weeks. Aspirin significantly reduced the number and size of colorectal tumors. Aspirin also significantly decreased tumor necrosis factor alpha and reactive oxygen species (ROS) levels in the plasma. Immunohistochemical analyses and western blots showed that cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), and the active form of Yes-associated protein 1 (YAP1), and cytosolic high mobility group box 1 (HMGB1) were strongly expressed at colorectal tumor sites and clearly suppressed by aspirin. An indicator of inflammation-related DNA damage, 8-nitroguanine, also accumulated in the colorectal tissues and was suppressed by aspirin. The present results suggest that the ingestion of aspirin suppressed carcinogenesis caused by inflammation through decreases in COX2 and ROS levels, resulting in reductions in DNA damage and oncogenic YAP1.</description><identifier>ISSN: 0912-0009</identifier><identifier>EISSN: 1880-5086</identifier><identifier>DOI: 10.3164/jcbn.20-189</identifier><identifier>PMID: 34857988</identifier><language>eng</language><publisher>Gifu: SOCIETY FOR FREE RADICAL RESEARCH JAPAN</publisher><subject>8-nitroguanine ; Aspirin ; Azoxymethane ; Cancer ; Carcinogenesis ; Carcinogens ; Colorectal cancer ; Colorectal carcinoma ; Cyclooxygenase-2 ; Damage accumulation ; Deoxyribonucleic acid ; Dextran ; Dextrans ; DNA ; DNA damage ; Epidemiology ; High mobility group proteins ; HMGB1 protein ; Inflammation ; Ingestion ; Nitric oxide ; Nitric-oxide synthase ; Oral administration ; Original ; Reactive oxygen species ; Risk analysis ; Risk factors ; Sodium sulfate ; Tumor necrosis factor-α ; Tumors ; Ulcerative colitis ; Western blotting ; Yes-associated protein ; yes-associated protein 1</subject><ispartof>Journal of Clinical Biochemistry and Nutrition, 2021, Vol.69(3), pp.265-271</ispartof><rights>2021 JCBN</rights><rights>2021. This work is published under https://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). 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Clin. Biochem. Nutr.</addtitle><description>Inflammation is a primary risk factor for cancer. Epidemiological studies previously demonstrated that aspirin decreased the incidence of cancer and specifically reduced the risk of colorectal cancer. However, the number of animal studies that have confirmed the efficacy of aspirin remains limited. Therefore, the purpose of the present study was to investigate the mechanisms by which aspirin prevents colorectal cancer in mice. ICR mice were treated with azoxymethane and the ulcerative colitis inducer, dextran sodium sulfate, to induce colorectal tumors. Aspirin was orally administered three times per week for 12 weeks. Aspirin significantly reduced the number and size of colorectal tumors. Aspirin also significantly decreased tumor necrosis factor alpha and reactive oxygen species (ROS) levels in the plasma. Immunohistochemical analyses and western blots showed that cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), and the active form of Yes-associated protein 1 (YAP1), and cytosolic high mobility group box 1 (HMGB1) were strongly expressed at colorectal tumor sites and clearly suppressed by aspirin. An indicator of inflammation-related DNA damage, 8-nitroguanine, also accumulated in the colorectal tissues and was suppressed by aspirin. The present results suggest that the ingestion of aspirin suppressed carcinogenesis caused by inflammation through decreases in COX2 and ROS levels, resulting in reductions in DNA damage and oncogenic YAP1.</description><subject>8-nitroguanine</subject><subject>Aspirin</subject><subject>Azoxymethane</subject><subject>Cancer</subject><subject>Carcinogenesis</subject><subject>Carcinogens</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Cyclooxygenase-2</subject><subject>Damage accumulation</subject><subject>Deoxyribonucleic acid</subject><subject>Dextran</subject><subject>Dextrans</subject><subject>DNA</subject><subject>DNA damage</subject><subject>Epidemiology</subject><subject>High mobility group proteins</subject><subject>HMGB1 protein</subject><subject>Inflammation</subject><subject>Ingestion</subject><subject>Nitric oxide</subject><subject>Nitric-oxide synthase</subject><subject>Oral administration</subject><subject>Original</subject><subject>Reactive oxygen species</subject><subject>Risk analysis</subject><subject>Risk factors</subject><subject>Sodium sulfate</subject><subject>Tumor necrosis factor-α</subject><subject>Tumors</subject><subject>Ulcerative colitis</subject><subject>Western blotting</subject><subject>Yes-associated protein</subject><subject>yes-associated protein 1</subject><issn>0912-0009</issn><issn>1880-5086</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNpdkUGLFDEQhYMo7uzqyT_Q4EWQXpN0dzq5CMugrrAggp5Dpboyk6E7GZOehf339tDLgF6qDu-rxyseY-8Ev22Eaj8d0MVbyWuhzQu2EVrzuuNavWQbboSsOefmil2XcuC8VZ1qX7OrptVdb7TesJ_bPU3pmOmR4hxSrNxTBeUYcogV7CDEMlch-hGmCc56nWmEmYYK05gy4QxjhRCR8oJVU0B6w155GAu9fd437PfXL7-29_XDj2_ft3cPNaqmm2s_tAJ651QrpZPaay-kN71WiM2AyksOyAdCObjOmYELL1E754Uj6Xovmxv2efU9ntxEAy75M4z2mMME-ckmCPZfJYa93aVHq5UQTWcWgw_PBjn9OVGZ7RQK0jhCpHQqViqujDS84wv6_j_0kE45Lu9Z2RnRql7JfqE-rhTmVEomfwkjuD1XZc9VWcntUtVC3630ocywowsLeQ440soqY5vzWG8uGu4hW4rNX8otoCM</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Ohnishi, Shiho</creator><creator>Hiramoto, Keiichi</creator><creator>Ma, Ning</creator><creator>Kawanishi, Shosuke</creator><general>SOCIETY FOR FREE RADICAL RESEARCH JAPAN</general><general>Japan Science and Technology Agency</general><general>the Society for Free Radical Research Japan</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7TK</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>2021</creationdate><title>Chemoprevention by aspirin against inflammation-related colorectal cancer in mice</title><author>Ohnishi, Shiho ; Hiramoto, Keiichi ; Ma, Ning ; Kawanishi, Shosuke</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c635t-fd41a7bb6422b28f8f12f9786cc3dc6f20ac0dec2db5b9d01f2c8bbf1be2b7f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>8-nitroguanine</topic><topic>Aspirin</topic><topic>Azoxymethane</topic><topic>Cancer</topic><topic>Carcinogenesis</topic><topic>Carcinogens</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Cyclooxygenase-2</topic><topic>Damage accumulation</topic><topic>Deoxyribonucleic acid</topic><topic>Dextran</topic><topic>Dextrans</topic><topic>DNA</topic><topic>DNA damage</topic><topic>Epidemiology</topic><topic>High mobility group proteins</topic><topic>HMGB1 protein</topic><topic>Inflammation</topic><topic>Ingestion</topic><topic>Nitric oxide</topic><topic>Nitric-oxide synthase</topic><topic>Oral administration</topic><topic>Original</topic><topic>Reactive oxygen species</topic><topic>Risk analysis</topic><topic>Risk factors</topic><topic>Sodium sulfate</topic><topic>Tumor necrosis factor-α</topic><topic>Tumors</topic><topic>Ulcerative colitis</topic><topic>Western blotting</topic><topic>Yes-associated protein</topic><topic>yes-associated protein 1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ohnishi, Shiho</creatorcontrib><creatorcontrib>Hiramoto, Keiichi</creatorcontrib><creatorcontrib>Ma, Ning</creatorcontrib><creatorcontrib>Kawanishi, Shosuke</creatorcontrib><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of Clinical Biochemistry and Nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ohnishi, Shiho</au><au>Hiramoto, Keiichi</au><au>Ma, Ning</au><au>Kawanishi, Shosuke</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chemoprevention by aspirin against inflammation-related colorectal cancer in mice</atitle><jtitle>Journal of Clinical Biochemistry and Nutrition</jtitle><addtitle>J. Clin. Biochem. Nutr.</addtitle><date>2021</date><risdate>2021</risdate><volume>69</volume><issue>3</issue><spage>265</spage><epage>271</epage><pages>265-271</pages><artnum>20-189</artnum><issn>0912-0009</issn><eissn>1880-5086</eissn><abstract>Inflammation is a primary risk factor for cancer. Epidemiological studies previously demonstrated that aspirin decreased the incidence of cancer and specifically reduced the risk of colorectal cancer. However, the number of animal studies that have confirmed the efficacy of aspirin remains limited. Therefore, the purpose of the present study was to investigate the mechanisms by which aspirin prevents colorectal cancer in mice. ICR mice were treated with azoxymethane and the ulcerative colitis inducer, dextran sodium sulfate, to induce colorectal tumors. Aspirin was orally administered three times per week for 12 weeks. Aspirin significantly reduced the number and size of colorectal tumors. Aspirin also significantly decreased tumor necrosis factor alpha and reactive oxygen species (ROS) levels in the plasma. Immunohistochemical analyses and western blots showed that cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), and the active form of Yes-associated protein 1 (YAP1), and cytosolic high mobility group box 1 (HMGB1) were strongly expressed at colorectal tumor sites and clearly suppressed by aspirin. An indicator of inflammation-related DNA damage, 8-nitroguanine, also accumulated in the colorectal tissues and was suppressed by aspirin. The present results suggest that the ingestion of aspirin suppressed carcinogenesis caused by inflammation through decreases in COX2 and ROS levels, resulting in reductions in DNA damage and oncogenic YAP1.</abstract><cop>Gifu</cop><pub>SOCIETY FOR FREE RADICAL RESEARCH JAPAN</pub><pmid>34857988</pmid><doi>10.3164/jcbn.20-189</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 8-nitroguanine Aspirin Azoxymethane Cancer Carcinogenesis Carcinogens Colorectal cancer Colorectal carcinoma Cyclooxygenase-2 Damage accumulation Deoxyribonucleic acid Dextran Dextrans DNA DNA damage Epidemiology High mobility group proteins HMGB1 protein Inflammation Ingestion Nitric oxide Nitric-oxide synthase Oral administration Original Reactive oxygen species Risk analysis Risk factors Sodium sulfate Tumor necrosis factor-α Tumors Ulcerative colitis Western blotting Yes-associated protein yes-associated protein 1 |
| title | Chemoprevention by aspirin against inflammation-related colorectal cancer in mice |
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