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Review
. 2017 Jan 3;8(1):1925-1936.
doi: 10.18632/oncotarget.12461.

Long non-coding RNAs in anti-cancer drug resistance

Qin-Nan Chen  1 , Chen-Chen Wei  1 , Zhao-Xia Wang  1 , Ming Sun  2
Affiliations
Review

Long non-coding RNAs in anti-cancer drug resistance

Qin-Nan Chen et al. Oncotarget. .

Abstract

Chemotherapy is one of the basic treatments for cancers; however, drug resistance is mainly responsible for the failure of clinical treatment. The mechanism of drug resistance is complicated because of interaction among various factors including drug efflux, DNA damage repair, apoptosis and targets mutation. Long non-coding RNAs (lncRNAs) have been a focus of research in the field of bioscience, and the latest studies have revealed that lncRNAs play essential roles in drug resistance in breast cancer, gastric cancer and lung cancer, et al. Dysregulation of multiple targets and pathways by lncRNAs results in the occurrence of chemoresistance. In this review, we will discuss the mechanisms underlying lncRNA-mediated resistance to chemotherapy and the therapeutic potential of lncRNAs in future cancer treatment.

Keywords: cancer; chemotherapy; drug resistance; long non-coding RNAs; targets.

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Conflict of interest statement

CONFLICTS OF INTEREST

None.

Figures

Figure 1
Figure 1. Overview of the involvement of long non-coding RNAs (lncRNAs) in cancer drug resistance
A. LncRNA-ATB competitively sponge miR-200c, downregulating ZEB1 expression, thus inducing trastuzumab resistance in breast cancer. B. GAS5 suppress the expression of phosphatase and tensin homologs (PTEN) by sponging miR-21. Downregulation of GAS5 leads to trastuzumab resistance in breast cancer. C. CCAL promotes MDR1 expression through activating Wnt/β-catenin pathway by targeting AP-2α in colorectal cancer. D. H19 induces MDR1 expression via increasing the MDR1 promoter methylation level in hepatocellular carcinoma.
See this image and copyright information in PMC

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