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Cellular irinotecan resistance in colorectal cancer and overcoming irinotecan refractoriness through various combination trials including DNA methyltransferase inhibitors: a review

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Cancer Drug Resistance 2021年第4期4卷 946-964页

作者： Shogo Ozawa Toshitaka Miura Jun Terashima wataru habano Division of Pharmacodynamics and Molecular Genetics School of PharmacyIwate Medical UniversityYahabaIwate 0283694Japan

Treatment with pharmacological drugs for colorectal cancer(CRC)remains unsatisfactory.A major cause of failure in pharmacotherapy is the resistance of colon cancer cells to the drugs,creating an urgent *** this review,we summarize previous studies on the resistance of CRC cells to irinotecan and discuss possible reasons for *** review presents the following five major causes of irinotecan resistance in human CRC:(1)cellular irinotecan resistance is induced mainly through the increased expression of the drug efflux transporter,ABCG2;(2)cellular irinotecan resistance is also induced in association with a nuclear receptor,pregnane/steroid X receptor(PXR/SXR),which is enriched in the CYP3A4 gene enhancer region in CRC cells by exposing the cells to SN-38;(3)irinotecan-resistant cells possess either reduced DNA topoisomerase I(Top1)expression at both the mRNA and protein levels or Top1 missense mutations;(4)alterations in the tumor microenvironment lead to drug resistance through intercellular vesicle-mediated transmission of miRNAs;and(5)CRC stem cells are the most difficult targets to successfully treat *** the clinical setting,CRC gradually develops resistance to initially effective irinotecan-based *** solve this problem,several clinical trials,such as irinotecan plus cetuximab *** monotherapy,have been *** clinical trial on irinotecan plus guadecitabine,a DNA-methyltransferase inhibitor,has also been conducted.

关键词： Drug resistance colorectal cancer anti-cancer drugs irinotecan ABCG2 DNA topoisomerase I cancer stem cells epigenetics

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对结肠直肠癌中SMAD4/DPC4多倍体基因改变的分析

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世界核心医学期刊文摘（胃肠病学分册） 2006年第2期2卷 26-27页

作者： Ando T. Sugai T. habano W. 李明 First Department of Internal Medicine Iwate Medical University Morioka 020- 8505 Japan

Background. Although recent animal studies have shown that SMAD4/DPC4 gene alterations are essential for late- stage intestinal tumorigenesis, the role of SMAD4/DPC4 gene alterations in primary human colorectal carcinomas is not fully understood. Therefore, we attempted to clarify the role of the SMAD4/DPC4 gene during tumor progression of colorectal carcinoma. Methods. Differences in allelic imbalance (AI) and mutations of the SMAD4/DPC4 gene between diploid and aneuploid populations were analyzed for 30 sporadic DNA multiploid colorectal carcinomas (used as a tumor progression model and defined as the coexistence of diploid and aneuploid cells within the same tumor). The crypt isolation technique was coupled with DNA cytometric sorting and a polymerase chain reaction assay. In addition, hypermethylation of the promoter region was examined to clarify whether inactivation of gene expression occurred. Results. Although a SMAD4/DPC4 gene AI was detected in only 5 of 27 informative diploid populations, 25 of 27 aneuploid populations had a SMAD4/DPC4 gene AI. Mutation of the SMAD4/DPC4 gene was detected in only one aneuploid population of multiploid colorectal carcinomas, but not in the corresponding diploid population. In total, 20 available multiploid carcinomas were selected for methylation analysis, and no evidence of hypermethylation of the promoter region was found. Conclusions. We suggest that, although mutation of the SMAD4/DPC4 gene and hypermethylation of the promoter region are infrequent events in colorectal tumorigenesis, AI at the SMAD4/DPC4 gene locus may play a key role in the progression of colorectal carcinomas.

关键词：结肠直肠癌 SMAD4/DPC4 基因突变肿瘤进展二倍体基因肠道肿瘤双倍体动物实验启动子

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