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本文引用的文献

1
Molecular mechanism of chemoresistance by miR-215 in osteosarcoma and colon cancer cells.miR-215 介导骨肉瘤和结肠癌耐药的分子机制。
Mol Cancer. 2010 Apr 30;9:96. doi: 10.1186/1476-4598-9-96.
2
MiR-24 tumor suppressor activity is regulated independent of p53 and through a target site polymorphism.miR-24 肿瘤抑制活性的调节独立于 p53 并通过靶位点多态性。
PLoS One. 2009 Dec 24;4(12):e8445. doi: 10.1371/journal.pone.0008445.
3
miR-24 Inhibits cell proliferation by targeting E2F2, MYC, and other cell-cycle genes via binding to "seedless" 3'UTR microRNA recognition elements.miR-24 通过与“无种子”3'UTR 微小 RNA 识别元件结合，靶向 E2F2、MYC 和其他细胞周期基因来抑制细胞增殖。
Mol Cell. 2009 Sep 11;35(5):610-25. doi: 10.1016/j.molcel.2009.08.020.
4
Mechanism of chemoresistance mediated by miR-140 in human osteosarcoma and colon cancer cells.miR-140介导的人骨肉瘤和结肠癌细胞化疗耐药机制。
Oncogene. 2009 Nov 19;28(46):4065-74. doi: 10.1038/onc.2009.274. Epub 2009 Sep 7.
5
Phenotypic subpopulations of metastatic colon cancer stem cells: genomic analysis.转移性结肠癌干细胞的表型亚群：基因组分析
Cancer Genomics Proteomics. 2009 Jan-Feb;6(1):19-29.
6
miR-192 Regulates dihydrofolate reductase and cellular proliferation through the p53-microRNA circuit.微小RNA-192通过p53-微小RNA信号通路调控二氢叶酸还原酶及细胞增殖。
Clin Cancer Res. 2008 Dec 15;14(24):8080-6. doi: 10.1158/1078-0432.CCR-08-1422.
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Coordinated regulation of cell cycle transcripts by p53-Inducible microRNAs, miR-192 and miR-215.由p53诱导的微小RNA miR-192和miR-215对细胞周期转录本的协同调控
Cancer Res. 2008 Dec 15;68(24):10105-12. doi: 10.1158/0008-5472.CAN-08-1846.
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p53-Responsive micrornas 192 and 215 are capable of inducing cell cycle arrest.对p53有反应的微小RNA 192和215能够诱导细胞周期停滞。
Cancer Res. 2008 Dec 15;68(24):10094-104. doi: 10.1158/0008-5472.CAN-08-1569.
9
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Oral Oncol. 2009 Jan;45(1):23-9. doi: 10.1016/j.oraloncology.2008.03.007. Epub 2008 May 19.
10
Evaluating the drug-target relationship between thymidylate synthase expression and tumor response to 5-fluorouracil. Is it time to move forward?评估胸苷酸合成酶表达与肿瘤对5-氟尿嘧啶反应之间的药物-靶点关系。是时候向前推进了吗？
Cancer Biol Ther. 2008 Jul;7(7):986-94. doi: 10.4161/cbt.7.7.6181. Epub 2008 Apr 21.

超越胸苷酸合成酶和二氢叶酸还原酶：非编码微小RNA在抗癌化疗耐药中的作用

Beyond Thymidylate Synthase and Dihydrofolate Reductase: Impact of Non-coding microRNAs in Anticancer Chemoresistance.

作者信息

Ju Jingfang

机构信息

Translational Research Laboratory, Department of Pathology, State University of New York at Stony Brook, Stony Brook, NY 11794-8691, USA.

出版信息

Curr Enzym Inhib. 2012 Sep 1;8(2):118-123. doi: 10.2174/157340812800793228.

DOI:10.2174/157340812800793228
PMID:24683387
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3966314/
Abstract

Chemoresistance is one of the major reasons for the failure of anticancer chemotherapy in treating advanced stage cancer. The mechanism of chemoresistance to fluoropyrimidines and antifolates has been extensively investigated in the past 40 years. It has been well established that thymidylate synthase (TYMS, TS) and dihydrofolate reductase (DHFR) are two major targets for fluoropyrimidines and antifolates, respectively. The regulatory mechanism of TS and DHFR expression is rather complex involving transcriptional, post-transcriptional and translational regulations. Our recent understanding of the chemoresistance mechanism has been extended beyond the simple one target/drug view. In this review, we will focus on the recent advancement of non-coding microRNAs (miRNAs) in contributing to the regulations of TS and DHFR expression, and to the chemoresistance mechanism of fluoropyrimidines and antifolates.

摘要

化疗耐药是晚期癌症抗癌化疗失败的主要原因之一。在过去40年里，对氟嘧啶和抗叶酸剂化疗耐药机制进行了广泛研究。已经明确胸苷酸合成酶（TYMS，TS）和二氢叶酸还原酶（DHFR）分别是氟嘧啶和抗叶酸剂的两个主要靶点。TS和DHFR表达的调控机制相当复杂，涉及转录、转录后和翻译调控。我们最近对化疗耐药机制的理解已超越了简单的单靶点/药物观点。在本综述中，我们将重点关注非编码微小RNA（miRNA）在调控TS和DHFR表达以及氟嘧啶和抗叶酸剂化疗耐药机制方面取得的最新进展。