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Published on: September 10, 2014
miR-181b/Notch2 overcome chemoresistance by regulating cancer stem cell-like properties in NSCLC
Xiaoyuan Wang1, Qingwei Meng1, Wenbo Qiao2
1The Department of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang Province, China.
Background:
Lung cancer stem cells have the ability to self-renew and are resistant to conventional chemotherapy. MicroRNAs (miRNAs) regulate and control the expression and function of many target genes; therefore, miRNA disorders are involved in the pathogenesis of human diseases, such as cancer. However, the effects of miRNA dysregulation on tumour stemness and drug resistance have not been fully elucidated. miR-181b has been reported to be a tumour suppressor miRNA and is associated with drug-resistant non-small cell lung cancer.
Methods:
Cancer stem cell (CSC)-like properties were tested by a cell proliferation assay and flow cytometry; miR-181b expression was measured by real-time PCR; and Notch2 and related proteins were detected by Western blotting and immunohistochemistry. A mouse xenograft model was also established.
Results:
In this study, we found that ectopic miR-181b expression suppressed cancer stem cell properties and enhanced sensitivity to cisplatin (DDP) treatment by directly targeting Notch2. miR-181b could inactivate the Notch2/Hes1 signalling pathway. In addition, tumours from nude mice treated with miR-181b were significantly smaller than tumours from mice treated with control agomir. Decreased miR-181b expression and increased Notch2 expression were observed to have a significant relationship with overall survival (OS) and CSC-like properties in non-small cell lung cancer (NSCLC) patients.
Conclusions:
This study elucidates an important role of miR-181b in the regulation of CSC-like properties, suggesting a potential therapeutic target for overcoming drug resistance in NSCLC.
Insights
MicroRNA-181b suppresses lung cancer stem cell traits and drug resistance by targeting Notch2. Restoring miR-181b may offer a new strategy for treating non-small cell lung cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Lung cancer stem cells (CSCs) exhibit self-renewal and chemoresistance.
- MicroRNA (miRNA) dysregulation contributes to cancer pathogenesis.
- The specific role of miRNA dysregulation in CSC stemness and drug resistance remains unclear.
Purpose of the Study:
- To investigate the role of miR-181b in regulating cancer stem cell (CSC)-like properties and chemoresistance in non-small cell lung cancer (NSCLC).
- To explore the therapeutic potential of miR-181b in overcoming drug resistance in NSCLC.
Main Methods:
- Assessed CSC-like properties using cell proliferation assays and flow cytometry.
- Quantified miR-181b expression via real-time PCR.
- Detected Notch2 and related proteins using Western blotting and immunohistochemistry.
- Utilized a mouse xenograft model to evaluate therapeutic efficacy.
Main Results:
- Ectopic miR-181b expression reduced CSC properties and increased sensitivity to cisplatin (DDP) by directly targeting Notch2.
- miR-181b inactivated the Notch2/Hes1 signaling pathway.
- Tumor growth was significantly inhibited in mice treated with miR-181b.
- Decreased miR-181b and increased Notch2 expression correlated with poorer overall survival and enhanced CSC properties in NSCLC patients.
Conclusions:
- miR-181b plays a crucial role in regulating CSC-like properties and chemoresistance in NSCLC.
- Targeting miR-181b presents a potential therapeutic strategy for overcoming drug resistance in NSCLC.
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