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Updated: Aug 21, 2025
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
miR-137 represses migration and cell motility by targeting COX-2 in non-small cell lung cancer
Yutu Luo1,2, Suwei Hu3, Fang Wang1
1Clinical Medical School of Yangzhou University, Subei People's Hospital of Jiangsu Province, Yangzhou, China.
Background:
Lung cancer is a common malignant tumor, with, non-small cell lung cancer (NSCLC) accounting for about 80-85% of cases. This study investigated the expression of miR-137 in NSCLC tissues and cells and its effects on the migration and invasion of NSCLC cells and related mechanisms.
Methods:
We collected the neoplastic and paracancerous tissues of NSCLC patients, detected the expression of miR-137 in NSCLC tissues and cell lines by real-time quantitative polymerase chain reaction (RT-qPCR), and analyzed the correlation between miR-137 expression and the clinicopathological features and survival of NSCLC. Following transfection with miR-137 mimic or inhibitor in NSCLC cell lines (A549 or H1299) to upregulate or downregulate the expression of miR-137, transwell assay was employed to detect the effects of miR-137 on migration or invasion. Online software was employed to predict and analyze the target gene of miR-137, and luciferase reporter gene system was adopted to validate it. The effects of miR-137 on the expressions of COX-2 and Epithelial-Mesenchymal Transition (EMT) related proteins were investigated by Western blot.
Results:
Compared to paracancerous tissues and BEAS-2B cells, the expressions of miR-137 in NSCLC tissues, A549 and H1299 cells were dramatically down-regulated (P<0.01). After transfection with miR-137 mimic or inhibitor in A549 and H1299 cells, the miR-137 expressions were markedly up-regulated or down-regulated (P<0.01), respectively. The number of migrating or invading cells was observably decreased or increased (P<0.01) after transfected with mimic or inhibitor, respectively, while relative luciferase activity was evidently decreased in cells co-transfected with miR-137 mimic and wild type recombined vector of 3'UTR of COX-2. While the expressions of COX-2 and E-cadherin were both substantially reduced in A549 cells treated with miR-137 mimic, that of vimentin was substantially raised. The expression of miR-137 correlated with smoking history, lymph node metastasis, and TNM clinical stage, and patients with high miR-137 expression had apparent longer survival.
Conclusions:
The expression of miR-137 was significantly down-regulated in NSCLC tissues and cells, and correlated with NSCLC progress. miR-137 suppressed the migration and invasion of NSCLC cells through regulating EMT relative proteins by targeting COX-2. miR-137 is expected to become a novel biomarker and therapeutic target of NSCLC.
Insights
MicroRNA-137 (miR-137) is significantly down-regulated in non-small cell lung cancer (NSCLC), suppressing tumor cell migration and invasion. This finding suggests miR-137 is a potential biomarker and therapeutic target for NSCLC.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Non-small cell lung cancer (NSCLC) is the most common type of lung cancer.
- The role of microRNA-137 (miR-137) in NSCLC progression requires further investigation.
Purpose of the Study:
- To investigate the expression levels of miR-137 in NSCLC.
- To determine the effects of miR-137 on NSCLC cell migration and invasion.
- To elucidate the underlying molecular mechanisms, including the targeting of COX-2 and regulation of Epithelial-Mesenchymal Transition (EMT).
Main Methods:
- Real-time quantitative polymerase chain reaction (RT-qPCR) to measure miR-137 expression in NSCLC tissues and cell lines.
- Transwell assays to assess cell migration and invasion after miR-137 modulation.
- Western blotting to analyze protein expression related to EMT and COX-2.
- Luciferase reporter gene assays to validate COX-2 as a direct target of miR-137.
Main Results:
- miR-137 expression was significantly downregulated in NSCLC tissues and cell lines compared to normal controls.
- Upregulating miR-137 (using mimic) decreased NSCLC cell migration and invasion, while downregulating it (using inhibitor) increased these processes.
- miR-137 directly targeted COX-2, and its upregulation suppressed COX-2 expression and key EMT markers (e.g., reduced vimentin, increased E-cadherin).
- Downregulated miR-137 expression correlated with smoking history, lymph node metastasis, and advanced TNM stage, with higher miR-137 levels associated with longer patient survival.
Conclusions:
- miR-137 plays a crucial role in suppressing NSCLC progression by inhibiting cell migration and invasion.
- The mechanism involves targeting COX-2 and modulating EMT-related proteins.
- miR-137 holds promise as a novel diagnostic biomarker and therapeutic target for NSCLC.
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