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Updated: Apr 25, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
miR-141 suppresses the growth and metastasis of HCC cells by targeting E2F3
Jun Xue1, Yan-Feng Niu, Jing Huang
1Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Abstract:
MicroRNAs (miRNAs) function as essential post-transcriptional modulators of gene expression involved in a wide range of physiologic and pathologic states, including cancer. Numerous miRNAs have been deregulated in hepatocellular carcinoma (HCC). Here, we investigated the role of miR-141 in HCC. Decreased expression of miR-141 was observed in both HCC tissues and cell lines. Ectopic overexpression of miR-141 reduced proliferation, migration, and invasion of HCC cells. E2F transcription factor 3 (E2F3) was confirmed to be a target of miR-141 in HCC cells. Moreover, restoration of E2F3 significantly reversed the tumor suppressive effects of miR-141. Our results suggest a critical role of miR-141 in suppressing metastasis of HCC cells by targeting E2F3.
Insights
MicroRNAs (miRNAs) are key in gene regulation and cancer. This study shows miR-141 suppresses hepatocellular carcinoma (HCC) metastasis by targeting E2F3, offering potential therapeutic insights.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are crucial post-transcriptional regulators of gene expression.
- Aberrant miRNA expression is implicated in various cancers, including hepatocellular carcinoma (HCC).
- The specific role of miR-141 in HCC progression and metastasis remains to be fully elucidated.
Purpose of the Study:
- To investigate the function of miR-141 in hepatocellular carcinoma (HCC).
- To identify the molecular targets of miR-141 in HCC.
- To determine the therapeutic potential of miR-141 in HCC treatment.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to assess miR-141 expression levels in HCC tissues and cell lines.
- In vitro assays (proliferation, migration, invasion) to evaluate the functional impact of miR-141.
- Western blotting and luciferase reporter assays to confirm E2F3 as a direct target of miR-141.
Main Results:
- miR-141 expression was significantly downregulated in HCC tissues and cell lines compared to normal controls.
- Overexpression of miR-141 inhibited HCC cell proliferation, migration, and invasion.
- E2F transcription factor 3 (E2F3) was validated as a direct downstream target of miR-141.
- Re-expression of E2F3 rescued the tumor-suppressive effects induced by miR-141 restoration.
Conclusions:
- miR-141 acts as a tumor suppressor in hepatocellular carcinoma.
- The miR-141/E2F3 axis plays a critical role in regulating HCC cell metastasis.
- Targeting miR-141 may represent a novel therapeutic strategy for inhibiting HCC progression.
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