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Updated: Apr 18, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MiR-204-5p suppresses cell proliferation by inhibiting IGFBP5 in papillary thyroid carcinoma
Lianyong Liu1, Jingnan Wang1, Xiangqi Li1
1Department of Endocrine, Shanghai Pudong Gongli Hospital, Shanghai 200135, China.
Abstract:
microRNAs (miRNAs) are frequently dysregulated in human malignancies. It was recently shown that miR-204-5p is downregulated in papillary thyroid carcinoma (PTC); however, the functional significance of this observation is not known. This study investigated the role of miR-204-5p in PTC. Overexpressing miR-204-5p suppressed PTC cell proliferation and induced cell cycle arrest and apoptosis. The results of a luciferase reporter assay showed that miR-204-5p can directly bind to the 3' untranslated region (UTR) of insulin-like growth factor-binding protein 5 (IGFBP5) mRNA, and IGFBP5 overexpression partially reversed the growth-inhibitory effects of miR-204-5p. These results indicate that miR-204-5p acts as a tumor suppressor in PTC by regulating IGFBP5 expression and that miR-204-5p can potentially serve as an antitumorigenic agent in the treatment of PTC.
Insights
MicroRNAs (miRNAs) like miR-204-5p suppress papillary thyroid carcinoma (PTC) growth by targeting IGFBP5. This finding suggests miR-204-5p as a potential therapeutic agent for PTC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are crucial regulators of gene expression, frequently altered in human cancers.
- miR-204-5p is notably downregulated in papillary thyroid carcinoma (PTC), but its functional role remains unclear.
Purpose of the Study:
- To investigate the functional significance of miR-204-5p in papillary thyroid carcinoma.
- To elucidate the molecular mechanisms underlying miR-204-5p's action in PTC.
Main Methods:
- Overexpression of miR-204-5p in PTC cell lines.
- Cell proliferation, cell cycle, and apoptosis assays.
- Luciferase reporter assay to confirm direct target binding.
- Insulin-like growth factor-binding protein 5 (IGFBP5) overexpression experiments.
Main Results:
- Overexpression of miR-204-5p significantly inhibited PTC cell proliferation.
- miR-204-5p induced cell cycle arrest and promoted apoptosis in PTC cells.
- miR-204-5p directly targets the 3' untranslated region (UTR) of IGFBP5 mRNA.
- IGFBP5 overexpression partially rescued the tumor-suppressive effects of miR-204-5p.
Conclusions:
- miR-204-5p functions as a tumor suppressor in papillary thyroid carcinoma.
- The tumor-suppressive activity of miR-204-5p is mediated through the regulation of IGFBP5 expression.
- miR-204-5p holds potential as an antitumorigenic agent for PTC therapy.
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