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Updated: May 8, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Long non-coding RNA MIR22HG impedes the progression of anaplastic thyroid carcinoma via targeting miR-141-3p/PTEN/AKT
Junyu Cao1, Peng Jiang2, Songliang Jiang2
1Department of Breast and Thyroid Surgery, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan, China. junyucao@kust.edu.cn.
Introduction:
Anaplastic thyroid carcinoma (ATC) is one of the most aggressive and lethal malignancies. The MiR-22 host gene (MIR22HG) has been identified as a novel long non-coding RNA (lncRNA) in a few types of cancer. Nevertheless, little is known about the potential role of MIR22HG in ATC. In this study, we aimed to investigate the biological functions and underlying molecular mechanisms of MIR22HG in ATC.
Material And Methods:
The expression of MIR22HG in tissues and cells of ATC were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The cell viabilities and invasive abilities were evaluated by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay, wound healing assay, and Matrigel invasion assay. The mechanism of MIR22HG interacting with microRNA-141-3p (miR-141-3p) was measured by RNA immunoprecipitation (RIP) assay, RNA pull-down assay, and dual-luciferase reporter assay.
Results:
MIR22HG was downregulated in ATC tissues and cells. More importantly, decreased expression of MIR22HG was found to be correlated with poor prognosis of ATC patients. Functional analysis showed that overexpression of MIR22HG attenuated the proliferation and metastasis of ATC both in vitro and in vivo. Mechanistically, MIR22HG positively modulated phosphatase and tensin homolog deleted on chromosome ten (PTEN) expression via sponging miR-141-3p, thus inhibiting downstream protein kinase B (AKT) signaling cascade.
Conclusions:
MIR22HG serves as a tumor suppressor in ATC and impedes the progression of ATC through regulation of miR-141-3p/PTEN/AKT axis. Our findings illustrate the critical role of the MIR22HG/miR-141-3p/PTEN/AKT axis in the progression of ATC, which offers new insights for the therapeutic strategies of ATC.
Insights
The long non-coding RNA MIR22HG acts as a tumor suppressor in anaplastic thyroid carcinoma (ATC). Its downregulation promotes ATC progression by affecting the miR-141-3p/PTEN/AKT pathway, offering new therapeutic targets.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Anaplastic thyroid carcinoma (ATC) is a highly aggressive and lethal cancer.
- The long non-coding RNA MIR22HG is implicated in various cancers, but its role in ATC is unclear.
Purpose of the Study:
- To investigate the function and molecular mechanisms of MIR22HG in anaplastic thyroid carcinoma.
- To explore MIR22HG as a potential therapeutic target for ATC.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to assess MIR22HG expression.
- In vitro and in vivo assays (MTT, wound healing, Matrigel invasion) to evaluate cell proliferation and metastasis.
- RNA immunoprecipitation (RIP), RNA pull-down, and dual-luciferase reporter assays to elucidate molecular interactions.
Main Results:
- MIR22HG expression was significantly downregulated in ATC tissues and cells.
- Lower MIR22HG levels correlated with poorer prognosis in ATC patients.
- Overexpression of MIR22HG suppressed ATC cell proliferation and metastasis.
- MIR22HG positively regulated PTEN by sponging miR-141-3p, inhibiting the AKT signaling pathway.
Conclusions:
- MIR22HG functions as a tumor suppressor in ATC.
- The MIR22HG/miR-141-3p/PTEN/AKT axis is critical in ATC progression.
- Targeting this axis may offer novel therapeutic strategies for ATC.
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