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The relationship between miR-17-5p, miR-92a, and let-7b expression with non-small cell lung cancer targeted drug
Jianhua Gong1, Li He, Jingping Ma
1Department of Respiratory Medicine, Jingzhou Central Hospital, Jingzhou Hubei, 434020, PR China.
Purpose:
To investigate the relationship between microRNA (miR)-17-5p, miR-92a, and let-7b expression and resistance to the non-small cell lung cancer (NSCLC) targeted drug Gefitinib.
Methods:
The human NSCLC cell line A549 and its drug resistant strain A549/GR (Gefitinib Resistant) was used in this study. The expression of miR-17-5p, miR-92a, and let-7b in different NSCLC cell lines was detected before and after transfection using real-time fluorescent PCR. Cell viability was detected using the CCK8 method. Cell cloning was performed to examine cell proliferation; cell apoptosis before and after transfection was evaluated using flow cytometry.
Results:
miR-17-5p and miR-92a expression in A549/ GR cells was 3.23 ± 0.92 and 9.29 ± 3.13 fold higher than in A549 cells respectively (p<0.05). In addition, let-7b expression in A549/GR cells was 29.37 ± 9.32% fold higher than in A549 cells (p<0.05). A549 cell sensitivity to Gefitinib was significantly decreased after transfection with the miR-17-5p mimic, miR-92a mimic, or the let-7b inhibitor (p<0.05), whereas the sensitivity of A549/GR cells to Gefitinib was significantly increased after transfection with miR-17-5p inhibitor, miR-92a inhibitor, or the let-7b mimic (p<0.05). A549 transfected with miR-17-5p mimic, miR- 92a mimic, and/or let-7b inhibitor formed more colonies than non-transfected controls (p<0.05); A549/GR transfected with miR-17-5p inhibitor, miR-92a inhibitor and let-7b mimic formed fewer colonies than the control group (p<0.05). The apoptosis rate of A549 cells transfected with miR-17-5p mimic, miR-92a mimic, or let-7b inhibitor was significantly lower than that of the control group (p<0.05); the apoptosis rate of A549/GR cells transfected with miR- 17-5p inhibitor, miR-92a inhibitor, or let-7b mimic was significantly higher than that of the control group (p<0.05).
Conclusions:
Increased miR-17-5p and miR-92a expression and decreased let-7b expression can significantly induce proliferation and inhibit apoptosis of lung cancer cells, while reducing lung cancer cell sensitivity to Gefitinib.
Insights
MicroRNA (miR)-17-5p and miR-92a upregulation, along with let-7b downregulation, promotes non-small cell lung cancer (NSCLC) cell proliferation and Gefitinib resistance. Modulating these microRNAs impacts Gefitinib sensitivity and apoptosis in NSCLC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality.
- Gefitinib is a targeted therapy for NSCLC, but drug resistance remains a significant clinical challenge.
- MicroRNAs (miRNAs) play crucial roles in cancer development and drug resistance.
Purpose of the Study:
- To investigate the association between microRNA (miR)-17-5p, miR-92a, and let-7b expression levels and Gefitinib resistance in NSCLC.
- To determine the functional impact of these miRNAs on Gefitinib sensitivity, cell proliferation, and apoptosis in NSCLC cells.
Main Methods:
- Utilized the human NSCLC cell line A549 and its Gefitinib-resistant counterpart A549/GR.
- Quantified miR-17-5p, miR-92a, and let-7b expression using real-time fluorescent PCR.
- Assessed cell viability (CCK8 assay), proliferation (colony formation assay), and apoptosis (flow cytometry) following miRNA transfections.
Main Results:
- A549/GR cells exhibited significantly higher expression of miR-17-5p (3.23-fold) and miR-92a (9.29-fold), and lower let-7b expression compared to A549 cells (p<0.05).
- Transfection with miR-17-5p or miR-92a mimics, or a let-7b inhibitor, decreased Gefitinib sensitivity and increased proliferation/colony formation in A549 cells.
- Conversely, inhibiting miR-17-5p or miR-92a, or using a let-7b mimic, increased Gefitinib sensitivity and induced apoptosis in A549/GR cells.
Conclusions:
- Upregulated miR-17-5p and miR-92a, coupled with downregulated let-7b, contribute to Gefitinib resistance in NSCLC by promoting proliferation and inhibiting apoptosis.
- Targeting these specific miRNAs holds potential for overcoming Gefitinib resistance in NSCLC treatment.
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