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Updated: Nov 2, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MicroRNA-17-5p inhibits thyroid cancer progression by suppressing Early growth response 2 (EGR2)
Xiang Geng1, YangYang Sun2, JinJin Fu3
1Department of Thyroid and Breast Surgery, The Affiliated Changzhou No.2 People's Hospital of Nanjing Medical University, Changzhou, China.
Abstract:
miR-17-5p has been proved that play important roles in many kinds of tumors progression. This study aimed at explore the function and mechanism of miR-17-5p in thyroid cancer (TC). RT-qPCR was used to detect miR-17-5p and Early growth response 2 (EGR2) expression in TC tissues and cells. CCK8 and colony formation assay were used to analyze cell proliferation. Cell migration and cell invasion was detected by Wound-healing assay and Transwell assay. Detection of protein expression using Western blot analysis. Dual-Luciferase assay was used to analyze the relationship between miR-17-5p and EGR2. In vivo experiment was performed by establishing Xenograft animal model to observe the function of miR-17-5p. We found that miR-17-5p is significantly increased in thyroid cancer tissues and cells. miR-17-5p inhibition repressed cell proliferation, clonal formation, cell migration, and cell invasion in thyroid carcinoma. Moreover, miR-17-5p inhibition suppressed tumorigenesis in vivo. Dual-Luciferase assay and Western blotting assay further proved that miR-17-5p has a negative regulation to EGR2. EGR2 was decreased in TC tissues and cells. Overexpressed EGR2 inhibited the development of thyroid carcinoma both vivo and in vivo. EGR2 knockdown remarkably decreased the anti-cancer effect of miR-17-5p inhibition. miR-17-5p is a thyroid cancer oncomir by modulation of the EGR2.
Insights
MicroRNA-17-5p (miR-17-5p) acts as an oncomiR in thyroid cancer, promoting tumor growth by suppressing Early Growth Response 2 (EGR2). Inhibiting miR-17-5p halts cancer progression and tumorigenesis.
Area of Science:
- Molecular Oncology
- Cancer Biology
Background:
- MicroRNAs (miRNAs) are key regulators in tumorigenesis.
- miR-17-5p is implicated in various cancer progressions.
- The role of miR-17-5p in thyroid cancer (TC) requires further elucidation.
Purpose of the Study:
- To investigate the function and mechanism of miR-17-5p in thyroid cancer.
- To determine the relationship between miR-17-5p and Early Growth Response 2 (EGR2) in TC.
Main Methods:
- Quantitative reverse transcription PCR (RT-qPCR) for gene expression analysis.
- Cell proliferation, migration, and invasion assays (CCK8, colony formation, wound-healing, Transwell).
- Western blot, Dual-Luciferase assay, and Xenograft animal models for mechanistic and in vivo studies.
Main Results:
- miR-17-5p expression was significantly upregulated in TC tissues and cells.
- Inhibition of miR-17-5p suppressed TC cell proliferation, migration, invasion, and in vivo tumorigenesis.
- miR-17-5p negatively regulated EGR2, which was downregulated in TC.
- EGR2 overexpression inhibited TC development, and its knockdown abrogated the anti-cancer effects of miR-17-5p inhibition.
Conclusions:
- miR-17-5p functions as a thyroid cancer oncomiR by modulating EGR2.
- Targeting the miR-17-5p/EGR2 axis presents a potential therapeutic strategy for thyroid cancer.
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