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Cell Cycle. 2013 May 1;12(9):1385-94. doi: 10.4161/cc.24477. Epub 2013 Apr 8.
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Downregulation of miRNA-31 induces taxane resistance in ovarian cancer cells through increase of receptor tyrosine kinase MET.miRNA-31 下调通过增加受体酪氨酸激酶 MET 诱导卵巢癌细胞对紫杉烷类药物耐药。
Oncogenesis. 2013 Mar 25;2(3):e40. doi: 10.1038/oncsis.2013.3.
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IMP3 protein promotes chemoresistance in breast cancer cells by regulating breast cancer resistance protein (ABCG2) expression.IMP3 蛋白通过调节乳腺癌耐药蛋白(ABCG2)的表达促进乳腺癌细胞的耐药性。
J Biol Chem. 2013 May 3;288(18):12569-73. doi: 10.1074/jbc.C112.442319. Epub 2013 Mar 28.
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The structure of the ARE-binding domains of Hu antigen R (HuR) undergoes conformational changes during RNA binding.Hu抗原R(HuR)的ARE结合结构域在与RNA结合过程中会发生构象变化。
Acta Crystallogr D Biol Crystallogr. 2013 Mar;69(Pt 3):373-80. doi: 10.1107/S0907444912047828. Epub 2013 Feb 16.
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MiR-200c and HuR in ovarian cancer.miR-200c 和 HuR 在卵巢癌中的作用。
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Mol Pharmacol. 2013 Apr;83(4):857-69. doi: 10.1124/mol.112.082743. Epub 2013 Jan 25.
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Adrenaline promotes cell proliferation and increases chemoresistance in colon cancer HT29 cells through induction of miR-155.肾上腺素通过诱导 miR-155 促进结肠癌 HT29 细胞的增殖并增加化疗耐药性。
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核糖核蛋白复合物在后转录水平调控获得性药物耐药性。

Post-transcriptional controls by ribonucleoprotein complexes in the acquisition of drug resistance.

机构信息

Department of Biochemistry, College of Medicine, Catholic University of Korea, Seoul 137-701, Korea.

出版信息

Int J Mol Sci. 2013 Aug 20;14(8):17204-20. doi: 10.3390/ijms140817204.

DOI:10.3390/ijms140817204
PMID:23965981
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3759960/
Abstract

Acquisition of drug resistance leads to failure of anti-cancer treatments and therapies. Although several successive chemotherapies are available, along with efforts towards clinical applications of new anti-cancer drugs, it is generally realized that there is a long way to go to treat cancers. Resistance to anti-cancer drugs results from various factors, including genetic as well as epigenetic differences in tumors. Determining the molecular and cellular mechanisms responsible for the acquisition of drug resistance may be a helpful approach for the development of new therapeutic strategies to overcome treatment failure. Several studies have shown that the acquisition of drug resistance is tightly regulated by post-transcriptional regulators such as RNA binding proteins (RBPs) and microRNAs (miRNAs), which change the stability and translation of mRNAs encoding factors involved in cell survival, proliferation, epithelial-mesenchymal transition, and drug metabolism. Here, we review our current understanding of ribonucleoprotein complexes, including RBPs and miRNAs, which play critical roles in the acquisition of drug resistance and have potential clinical implications for cancer.

摘要

耐药性的获得导致抗癌治疗和疗法的失败。尽管有几种连续的化疗药物以及新抗癌药物的临床应用的努力,但人们普遍认识到,要治疗癌症还有很长的路要走。抗癌药物的耐药性是由多种因素引起的,包括肿瘤中的遗传和表观遗传差异。确定导致耐药性获得的分子和细胞机制可能有助于开发新的治疗策略来克服治疗失败。几项研究表明,药物耐药性的获得受到 RNA 结合蛋白 (RBPs) 和 microRNAs (miRNAs) 等转录后调节剂的严格调控,这些调节剂改变了参与细胞存活、增殖、上皮-间充质转化和药物代谢的编码因子的 mRNA 的稳定性和翻译。在这里,我们回顾了我们对核糖核蛋白复合物的理解,包括 RBP 和 miRNA,它们在耐药性的获得中发挥着关键作用,并对癌症具有潜在的临床意义。