Abstract

Lung cancer is one of main causes of cancer mortality and 83% of lung cancer cases are classified as non-small cell lung cancer (NSCLC). Patients with NSCLC usually have a poor prognosis and one of the leading causes is drug resistance. With the progress of drug therapy, the emergence and development of drug resistance affected the prognosis of patients severely. Accumulating evidence reveals that long non-coding RNAs (lncRNAs), as “dark matters” of the human genome, is of great significance to drug resistance in NSCLC. Herein, we review the role of lncRNAs in drug resistance in NSCLC.

Highlights

  • As one of the cancers with high incidence worldwide, lung cancer is the main cause of cancer mortality due to the high fatality related to the disease (Testa et al, 2018)

  • Reanalysis of gefitinib, erlotinib, and crizotinib resistance showed the alterations of many long non-coding RNAs (lncRNAs) in different EGFR-TKIs resistant nonsmall cell lung cancer (NSCLC) cells and qPCR validated the alterations of four lncRNAs in gefitinib-resistant PC9 cell line (Ma et al, 2017)

  • LncRNA GAS5 is downregulated in NSCLC cells and improves the sensitivity of NSCLC to drugs include cisplatin (DDP) lung cancer cells via miR-21/PTEN axis (Cao et al, 2017)

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Summary

INTRODUCTION

As one of the cancers with high incidence worldwide, lung cancer is the main cause of cancer mortality due to the high fatality related to the disease (Testa et al, 2018). Reanalysis of gefitinib, erlotinib, and crizotinib resistance showed the alterations of many lncRNAs in different EGFR-TKIs resistant NSCLC cells and qPCR validated the alterations of four lncRNAs in gefitinib-resistant PC9 cell line (Ma et al, 2017). Altered expression of lncRNAs results in abnormal signaling pathways and regulates effects of anti-cancer drugs (Jiang et al, 2018). There were several reviews focused on lncRNAs related to DDP and EGFR-TKIs resistance in lung cancer (Chen et al, 2016b; Wang et al, 2018). We review the role of lncRNAs in drug resistance to DDP, taxanes, and EGFRTKIs in NSCLC and summarize lncRNAs and resistance to other drugs targeting abnormally activated signaling pathways and attenuated immune response in NSCLC prospectively

LncRNAs and NSCLC DDP Resistance
Upregulated LncRNAs in NSCLC DDP Resistance
Downregulated LncRNAs in NSCLC DDP Resistance
LncRNAs and NSCLC Taxanes Resistance
Upregulated LncRNAs in NSCLC EGFRTKIs Resistance
Downregulated LncRNAs in NSCLC EGFRTKIs Resistance
LncRNAs and NSCLC Resistance to Other Drugs
Clinical Prospects of LncRNAs in NSCLC
CONCLUSIONS
Findings
AUTHOR CONTRIBUTIONS
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