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Updated: Oct 12, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MiR-186 Suppressed Growth, Migration, and Invasion of Lung Adenocarcinoma Cells via Targeting Dicer1
Juan Wang1, Yi Zhang2, Fanghong Ge3
1Department of Oncology, Tongzhou Hospital Affiliated to Nantong University, Nantong, Jiangsu 226300, China.
Objective:
Globally, the fatal form of lung cancer is non-small-cell lung cancer (NSCLC), and its most common subtype is lung adenocarcinoma (LUAD). In cancer development and progression, miRNAs play key roles primarily in interacting with cancer-related genes. The main focus of this research was to examine the biological roles of miR-186 in LUAD.
Methods:
We examined tissues of LUAD and lung cancer cell lines. The expressions of miR-186, Dicer1, Ki-67, and PCNA were determined by immunohistochemistry (IHC), real-time quantitative PCR (RT-PCR), and western blot assays. The CCK-8 and transwell assays were used to determine cell proliferation, migration, and invasion. To determine the association between miR-186 and Dicer1, a luciferase assay was used.
Results:
MiR-186 expression was found to be lower in LUAD tissues, and this was correlated to TNM stage and lymph node metastasis in LUAD patients. miR-186 upregulation significantly reduced the proliferation rate and the level of Ki67 and PCNA of LUAD cell lines HCC827 and A549. Transwell assay exhibited that miR-186 upregulation considerably reduced HCC827 and A549 cells' migration and invasion abilities. Furthermore, we also confirmed that Dicer1 was a direct target of miR-186. Importantly, Dicer1 overexpression abolished the suppression of miR-186 mimics on cell proliferation, migration, and invasion of HCC827 and A549 cells.
Conclusion:
These results indicated that the miR-186/Dicer1 pathway is critical for regulating LUAD cell proliferation, migration, and invasion.
Insights
MicroRNA-186 (miR-186) is downregulated in lung adenocarcinoma (LUAD). Restoring miR-186 inhibits LUAD cell proliferation, migration, and invasion by targeting Dicer1, suggesting a critical regulatory role.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Non-small-cell lung cancer (NSCLC), particularly lung adenocarcinoma (LUAD), is a leading cause of cancer mortality worldwide.
- MicroRNAs (miRNAs) are crucial regulators of gene expression involved in cancer development and progression.
- The specific role of miR-186 in LUAD pathogenesis requires further investigation.
Purpose of the Study:
- To investigate the biological functions of miR-186 in lung adenocarcinoma (LUAD).
- To elucidate the molecular mechanisms underlying miR-186's role in LUAD progression.
Main Methods:
- Analysis of miR-186 expression in LUAD tissues and cell lines using immunohistochemistry, RT-PCR, and western blot.
- Assessment of cell proliferation, migration, and invasion using CCK-8 and Transwell assays.
- Luciferase assays to confirm the direct targeting of Dicer1 by miR-186 and functional rescue experiments.
Main Results:
- Lower miR-186 expression was observed in LUAD tissues, correlating with advanced TNM stage and lymph node metastasis.
- Upregulation of miR-186 significantly suppressed LUAD cell proliferation, migration, and invasion.
- Dicer1 was identified as a direct target of miR-186, and its overexpression reversed the inhibitory effects of miR-186.
Conclusions:
- The miR-186/Dicer1 pathway plays a critical role in the regulation of LUAD cell proliferation, migration, and invasion.
- miR-186 functions as a tumor suppressor in LUAD.
- Targeting the miR-186/Dicer1 pathway may offer a potential therapeutic strategy for LUAD.
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