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[Advances in Long Non-coding RNAs on Resistant to EGFR-TKIs in Non-small Cell Lung Cancer]
Shubin Li1, Hong Yu2, Gengyue Zhang2
1Department of Internal Medicine, Southern Branch of Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 102600, China.
Abstract:
Most non-small cell lung cancer patients with active epidermal growth factor receptor (EGFR) mutation will eventually acquire drug resistant to EGFR tyrosine kinase inhibitors, such as gefitinib, resulting in disease progression, which involves a variety of complex mechanisms. Up to now, the molecular mechanisms of long non-coding RNAs mediated EGFR-TKIs resistance remains poorly understood. This review aims to outline the current state of information on lncRNAs and progress on its role in EGFR-TKIs resistance in non-small cell lung cancer.
Insights
Most non-small cell lung cancer patients develop resistance to EGFR tyrosine kinase inhibitors. This review explores the poorly understood role of long non-coding RNAs in mediating this drug resistance.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Non-small cell lung cancer (NSCLC) frequently harbors epidermal growth factor receptor (EGFR) mutations.
- Acquired resistance to EGFR tyrosine kinase inhibitors (TKIs) like gefitinib is a major cause of disease progression in NSCLC patients.
- The molecular mechanisms underlying EGFR-TKI resistance are complex and not fully elucidated.
Purpose of the Study:
- To review the current understanding of long non-coding RNAs (lncRNAs).
- To summarize the emerging role of lncRNAs in mediating resistance to EGFR-TKIs in NSCLC.
- To highlight knowledge gaps in lncRNA-mediated EGFR-TKI resistance.
Main Methods:
- Literature review
- Synthesis of current research findings
- Analysis of molecular mechanisms
Main Results:
- Long non-coding RNAs (lncRNAs) are increasingly recognized as key players in cancer development and progression.
- Evidence suggests that specific lncRNAs can influence EGFR-TKI sensitivity and resistance through various molecular pathways.
- Dysregulation of lncRNAs contributes to the complex mechanisms of acquired resistance.
Conclusions:
- lncRNAs represent a significant, yet understudied, factor in EGFR-TKI resistance in NSCLC.
- Further research into lncRNA function is crucial for understanding and overcoming treatment resistance.
- Targeting lncRNAs may offer novel therapeutic strategies for overcoming EGFR-TKI resistance in NSCLC.
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