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Updated: Aug 30, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MiR-504-3p Has Tumor-Suppressing Activity and Decreases IFITM1 Expression in Non-Small Cell Lung Cancer Cells
Zining Liu1,2,3, Weili Zhang2, Biao Zhang4
1Department of Respiratory Diseases, Suzhou Municipal Hospital, Suzhou, China.
Abstract:
Objective: To analyze the impact of expression of miR-504-3p on the proliferation, migration, cell cycle transit and rate of apoptosis of NSCLC cells and explore the underlying mechanisms. Methods: The Cancer Genome Atlas (TCGA) database was used to compare the expression levels of miR-504 between NSCLC tissues and normal lung tissues. NSCLC cells were transfected with lentiviral vectors that either overexpressed or knocked down miR-504-3p to evaluate its effects on NSCLC biological behavior. Quantitative Real Time Polymerase Chain Reaction was used to measure the levels of miR-504-3p and Interferon-Induced Transmembrane Protein 1 (IFITM1). A luciferase reporter array was used to reveal whether miR-504-3p directly targets IFITM1. Results: The expression of miR-504 was significantly down-regulated in lung cancer tissues compared to normal lung tissues. Overexpression of miR-504-3p in NSCLC cell lines inhibited cell proliferation, migration and promoted cell apoptosis. Meanwhile, changes in the expression level of miR-504-3p had no significant effect on NSCLC cell cycle progression. Moreover, over-expressed miR-504-3p following its transfection significantly decreased the expression of IFITM1 in NSCLC cell lines and suppressed the activity of the luciferase reporter containing wild type but not mutant IFITM1 3' -UTR. Conclusion: miR-504-3p inhibits cell proliferation and migration and promotes cell apoptosis in NSCLC cells. MiR-504-3p decreases IFITM1 expression in NSCLC cells, which may be a potential mechanism of its tumor-suppressive functions in NSCLC.
Insights
MicroRNA-504-3p (miR-504-3p) suppresses non-small cell lung cancer (NSCLC) growth by inhibiting proliferation and migration while promoting apoptosis. It achieves this by downregulating Interferon-Induced Transmembrane Protein 1 (IFITM1) expression.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality.
- MicroRNAs (miRNAs) play crucial roles in cancer development and progression.
- The specific role of miR-504-3p in NSCLC remains largely uncharacterized.
Purpose of the Study:
- To investigate the functional impact of miR-504-3p expression on NSCLC cell proliferation, migration, cell cycle, and apoptosis.
- To elucidate the underlying molecular mechanisms, including the potential target gene IFITM1.
- To analyze miR-504 expression patterns in NSCLC patient tissues.
Main Methods:
- Utilized The Cancer Genome Atlas (TCGA) database for comparative analysis of miR-504 expression in NSCLC versus normal tissues.
- Employed lentiviral vectors for overexpression and knockdown of miR-504-3p in NSCLC cell lines.
- Quantified gene expression using Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) for miR-504-3p and IFITM1.
- Validated direct targeting of IFITM1 by miR-504-3p using a luciferase reporter assay.
Main Results:
- miR-504-3p expression was significantly downregulated in NSCLC tissues compared to normal lung tissues.
- Overexpression of miR-504-3p inhibited NSCLC cell proliferation and migration and induced apoptosis.
- miR-504-3p overexpression did not significantly affect NSCLC cell cycle progression.
- miR-504-3p significantly decreased IFITM1 expression and luciferase activity in NSCLC cells, indicating direct targeting.
Conclusions:
- miR-504-3p acts as a tumor suppressor in NSCLC by inhibiting cell proliferation and migration and promoting apoptosis.
- The downregulation of IFITM1 by miR-504-3p is a key mechanism underlying its tumor-suppressive functions in NSCLC.
- miR-504-3p represents a potential therapeutic target for NSCLC treatment.
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