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Updated: Apr 19, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Down-regulation of miR-181b promotes apoptosis by targeting CYLD in thyroid papillary cancer
Dengfeng Li1, Wei Jian1, Chuankui Wei1
1Department of General Surgery, Shanghai 10th People's Hospital, School of Medicine, Tongji University Shanghai 200072, China.
Abstract:
MicroRNAs (miRNAs) are a small class of non-coding RNAs that are widely deregulated in various cancers. They act as either oncogenes or tumor suppressor genes in human cancer. The purpose of this study was to examine the potential role of miR-181b in human thyroid papillary cancer. The expression levels of different miRNAs were measured by micro array analysis in 10 thyroid papillary cancer specimens and adjacent normal thyroid cancer tissues. MTT assays, colony formation assays, apoptosis assays were used to explore the potential function of miR-181b inhibitor in TPC1 human thyroid papillary cancer cells. Luciferase reporter assays were performed to validate the regulation of a putative target of miR-181b, in corroboration with qPCR and western blot assays. We found that the expression of miR-181b was higher in thyroid papillary cancer specimens compared with adjacent normal tissues (P < 0.05). Downregulation of miR-181b inhibited cellular growth and promoted cellular apoptosis. Luciferase assays indicated that miR-181b can bind with its putative target site in the 3'-untranslated region (3'-UTR) of CYLD, suggesting that CYLD is a direct target of miR-181b. Western blot analysis indicated that downregulation of miR-181b results in the upregulation of CYLD at protein levels. Taken together, downregulation of miR-181b expression causes cellular growth inhibition, promoting cellular apoptosis by targeting CYLD. These findings suggest that downregulation of the expression of miR-181b may be a therapeutic target for the treatment of human thyroid papillary cancer.
Insights
MicroRNA 181b (miR-181b) is upregulated in thyroid cancer. Inhibiting miR-181b suppresses tumor growth and promotes apoptosis by targeting the CYLD gene, suggesting miR-181b as a potential therapeutic target.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- MicroRNAs (miRNAs) are key regulators of gene expression implicated in various cancers.
- Dysregulation of miRNAs, including acting as oncogenes or tumor suppressors, is common in human cancers.
- Thyroid papillary cancer (TPC) is a prevalent endocrine malignancy with complex molecular underpinnings.
Purpose of the Study:
- To investigate the role of miR-181b in the development and progression of human thyroid papillary cancer.
- To explore the functional impact of miR-181b downregulation on TPC cell behavior.
- To identify and validate the direct molecular targets of miR-181b in thyroid cancer cells.
Main Methods:
- Microarray analysis to compare miRNA expression in TPC tissues versus normal tissues.
- In vitro assays (MTT, colony formation, apoptosis) to assess the functional effects of miR-181b inhibition.
- Luciferase reporter assays, qPCR, and Western blot to validate miR-181b targets and downstream effects.
Main Results:
- miR-181b expression was significantly higher in thyroid papillary cancer tissues compared to adjacent normal tissues.
- Downregulation of miR-181b in TPC cells led to reduced cellular proliferation and induced apoptosis.
- Luciferase assays confirmed that CYLD is a direct target of miR-181b, with its protein expression upregulated upon miR-181b inhibition.
Conclusions:
- miR-181b promotes thyroid papillary cancer cell growth and inhibits apoptosis, at least partly by suppressing CYLD.
- Downregulation of miR-181b exhibits anti-cancer effects in thyroid papillary cancer.
- Targeting miR-181b represents a potential therapeutic strategy for human thyroid papillary cancer.
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