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微小 RNA 在胃癌多药耐药机制中的作用。

The Roles of microRNAs in Multidrug-Resistance Mechanisms in Gastric Cancer.

机构信息

Department of Gastroenterology, The First Hospital of Lanzhou University, Lanzhou, China.

Department of Gastroenterology, The first Hospital of Lanzhou University, Lanzhou, China.

出版信息

Curr Mol Med. 2020;20(9):667-674. doi: 10.2174/1566524020666200226124336.

DOI:10.2174/1566524020666200226124336
PMID:32209033
Abstract

Multidrug resistance (MDR) is one of the most significant reasons for the chemotherapeutics failure in gastric cancer. Although accumulating investigations and researches have been made to elucidate the mechanisms of multidrug resistance, the detail is far from completely understood. The importance of microRNAs in cancer chemotherapeutic resistance has been demonstrated recently, which provides a new strategy to overcome multidrug resistance. The different mechanisms are related to the phenomena of MDR itself and the roles of miRNAs in these multi-mechanisms by which MDR is acquired. In turn, the aim of this review was to summarize recent publications of microRNAs in regulating MDR in gastric cancer, thereby potentially developing as targeted therapies. Further unraveling the roles of microRNAs in MDR mechanisms including the ATP-binding cassette (ABC) transporter family, autophagy induction, cancer stem cell regulation, hypoxia induction, DNA damage and repair, epigenetic regulation, and exosomes in gastric cancer will be helpful for us to win the battle against it.

摘要

多药耐药(MDR)是胃癌化疗失败的最重要原因之一。尽管已经进行了大量的研究来阐明多药耐药的机制,但细节远未完全了解。最近已经证明了 microRNAs 在癌症化疗耐药性中的重要性,为克服多药耐药性提供了一种新的策略。不同的机制与 MDR 本身的现象以及 microRNAs 在这些多机制中获得 MDR 的作用有关。反过来,本综述的目的是总结 microRNAs 在调节胃癌多药耐药性中的最新研究进展,从而为靶向治疗提供潜在的靶点。进一步阐明 microRNAs 在包括 ABC 转运蛋白家族、自噬诱导、肿瘤干细胞调节、缺氧诱导、DNA 损伤和修复、表观遗传调控以及外泌体在内的 MDR 机制中的作用,将有助于我们赢得对抗它的战斗。

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Cancers (Basel). 2024 Apr 29;16(9):1729. doi: 10.3390/cancers16091729.
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The Role of Autophagy in Gastric Cancer Chemoresistance: Friend or Foe?自噬在胃癌化疗耐药中的作用:是友还是敌?
Front Cell Dev Biol. 2020 Dec 3;8:621428. doi: 10.3389/fcell.2020.621428. eCollection 2020.