CXCR2 Inhibition Enhances Sulindac-Mediated Suppression of Colon Cancer Development
Identifieur interne : 002C86 ( Main/Exploration ); précédent : 002C85; suivant : 002C87CXCR2 Inhibition Enhances Sulindac-Mediated Suppression of Colon Cancer Development
Auteurs : Yong Suk Lee [États-Unis] ; Dongwon Choi [États-Unis] ; Nam Yoon Kim [États-Unis] ; Sara Yang [États-Unis] ; Eunson Jung [États-Unis] ; Mingu Hong [États-Unis] ; Dongyun Yang [États-Unis] ; Heinz-Josef Lenz [États-Unis] ; Young-Kwon Hong [États-Unis]Source :
- International journal of cancer. Journal international du cancer [ 0020-7136 ] ; 2014.
Abstract
Small chemical compound sulindac has been approved as a preventive approach against colon cancer for its effectiveness in treatment of precancerous adenoma. Due to its severe toxicities in the cardiovascular, gastrointestinal and renal systems, however, a combination of low-dose sulindac with other chemopreventive agents has been sought after as an alternative therapeutic strategy that could increase its effectiveness, while minimizing its adverse effects. In order to identify the promising alternative approach, we investigated the therapeutic potential of targeting the Interleukin (IL)-8/CXCR2 pathway in colon cancer treatment using both loss-of-function (CXCR2 knockout) and gain-of-function (IL-8 overexpression) mouse models, as the IL-8/CXCR2 pathway has been shown to be activated in intestinal tumors of both human and experimental animals. We found that deletion of CXCR2 gene and ectopic expression of IL-8 suppresses and enhances, respectively, intestinal tumor development caused by a mutation in the APC gene. Moreover, a single copy deletion of CXCR2 gene resulted in abrogation of COX-2 and Gro-α upregulation in intestinal tumors caused by the APC mutation. Moreover, a single copy (heterozygote) deletion of CXCR2 gene was sufficient to synergize with a low-dose sulindac treatment in suppressing APCmin-induced intestinal polyposis. Together, our study provides a therapeutic justification of combined inhibition of CXCR2 and sulindac treatment in colon cancer prevention.
Url:
DOI: 10.1002/ijc.28668
PubMed: 24338666
PubMed Central: 4166491
Affiliations:
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<front><div type="abstract" xml:lang="en"><p id="P2">Small chemical compound sulindac has been approved as a preventive approach against colon cancer for its effectiveness in treatment of precancerous adenoma. Due to its severe toxicities in the cardiovascular, gastrointestinal and renal systems, however, a combination of low-dose sulindac with other chemopreventive agents has been sought after as an alternative therapeutic strategy that could increase its effectiveness, while minimizing its adverse effects. In order to identify the promising alternative approach, we investigated the therapeutic potential of targeting the Interleukin (IL)-8/CXCR2 pathway in colon cancer treatment using both loss-of-function (CXCR2 knockout) and gain-of-function (IL-8 overexpression) mouse models, as the IL-8/CXCR2 pathway has been shown to be activated in intestinal tumors of both human and experimental animals. We found that deletion of CXCR2 gene and ectopic expression of IL-8 suppresses and enhances, respectively, intestinal tumor development caused by a mutation in the APC gene. Moreover, a single copy deletion of CXCR2 gene resulted in abrogation of COX-2 and Gro-α upregulation in intestinal tumors caused by the APC mutation. Moreover, a single copy (heterozygote) deletion of CXCR2 gene was sufficient to synergize with a low-dose sulindac treatment in suppressing APCmin-induced intestinal polyposis. Together, our study provides a therapeutic justification of combined inhibition of CXCR2 and sulindac treatment in colon cancer prevention.</p>
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<name sortKey="Hong, Mingu" sort="Hong, Mingu" uniqKey="Hong M" first="Mingu" last="Hong">Mingu Hong</name>
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<name sortKey="Hong, Young Kwon" sort="Hong, Young Kwon" uniqKey="Hong Y" first="Young-Kwon" last="Hong">Young-Kwon Hong</name>
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<name sortKey="Kim, Nam Yoon" sort="Kim, Nam Yoon" uniqKey="Kim N" first="Nam Yoon" last="Kim">Nam Yoon Kim</name>
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<name sortKey="Yang, Dongyun" sort="Yang, Dongyun" uniqKey="Yang D" first="Dongyun" last="Yang">Dongyun Yang</name>
<name sortKey="Yang, Dongyun" sort="Yang, Dongyun" uniqKey="Yang D" first="Dongyun" last="Yang">Dongyun Yang</name>
<name sortKey="Yang, Sara" sort="Yang, Sara" uniqKey="Yang S" first="Sara" last="Yang">Sara Yang</name>
<name sortKey="Yang, Sara" sort="Yang, Sara" uniqKey="Yang S" first="Sara" last="Yang">Sara Yang</name>
</country>
</tree>
</affiliations>
</record>
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