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Updated: Mar 8, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MiR-125b inhibits anaplastic thyroid cancer cell migration and invasion by targeting PIK3CD
Qingao Bu1, Faping You1, Guozheng Pan1
1Shengli Oilfield Central Hospital, Jinan Road, Dongying, Shandong Province No. 31, 257034, China.
Abstract:
Emerging evidences indicate that dysregulated microRNAs are implicated in the process of tumorigenesis and progression. The miRNA-125b (miR-125b) is downregulated and identified as tumor supressor in various cancers including thyroid cancer. However, the role and mechanism of miR-125b in anaplastic thyroid cancer (ATC) migration and invasion remain unknown. In the present study, the expression levels of miR-125b were downregulated and the expression levels of phosphoinositide 3-kinase catalytic subunit delta (PIK3CD) were upregulated in ATC tissues and cell lines. Moreover, miR-125b expression was negatively related to PIK3CD expression in ATC tissues. A computational search and luciferase assay identified PIK3CD as a direct target of miR-125b in ATC and PIK3CD expression was downregulated by miR-125b in ATC cells. In terms of function, miR-125b repressed migration and invasion of ATC cells, whereas PIK3CD overexpression reversed this effect. Furthermore, we showed that exogenous miR-125b decreased the PI3K, phospho-Akt, and phospho-mTOR expression in ATC cells. In conclusion, these results indicated that miR-125b suppressed ATC cell migration and invasion by targeting PIK3CD expression, and suggested novel potential therapeutic targets for the treatment of ATC.
Insights
MicroRNA-125b (miR-125b) suppresses anaplastic thyroid cancer (ATC) cell migration and invasion by targeting phosphoinositide 3-kinase catalytic subunit delta (PIK3CD). This finding reveals miR-125b as a potential therapeutic target for ATC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Dysregulated microRNAs (miRNAs) are involved in cancer development and progression.
- MicroRNA-125b (miR-125b) acts as a tumor suppressor and is downregulated in various cancers, including thyroid cancer.
- The specific role and mechanism of miR-125b in anaplastic thyroid cancer (ATC) cell migration and invasion are not well understood.
Purpose of the Study:
- To investigate the role and mechanism of miR-125b in the migration and invasion of anaplastic thyroid cancer (ATC).
- To identify the molecular targets of miR-125b in ATC.
- To explore the therapeutic potential of targeting miR-125b in ATC.
Main Methods:
- Quantitative real-time PCR to measure miR-125b and phosphoinositide 3-kinase catalytic subunit delta (PIK3CD) expression in ATC tissues and cell lines.
- Bioinformatic analysis and luciferase reporter assays to confirm PIK3CD as a direct target of miR-125b.
- In vitro cell migration and invasion assays to assess the functional impact of miR-125b and PIK3CD.
- Western blot analysis to evaluate the effects of miR-125b on downstream signaling pathways (PI3K, Akt, mTOR).
Main Results:
- miR-125b was significantly downregulated, while PIK3CD was upregulated in ATC tissues and cell lines.
- miR-125b directly targeted and downregulated PIK3CD expression in ATC cells.
- Overexpression of miR-125b inhibited ATC cell migration and invasion, an effect reversed by PIK3CD overexpression.
- miR-125b suppressed the PI3K/Akt/mTOR signaling pathway in ATC cells.
Conclusions:
- miR-125b suppresses anaplastic thyroid cancer cell migration and invasion by targeting PIK3CD.
- The miR-125b/PIK3CD axis represents a potential therapeutic strategy for ATC.
- Targeting miR-125b may offer novel therapeutic avenues for anaplastic thyroid cancer treatment.
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