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Updated: Jan 22, 2026
Transoral Robotic Total Thyroidectomy and Bilateral Central Regional Lymph Node Dissection for Papillary Thyroid Carcinoma
Published on: September 15, 2023
MIR22HG inhibits cell growth, migration and invasion through regulating the miR-24-3p/p27kip1 axis in thyroid
1Department of Gastrointestinal and Gland Surgery, the First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China. go60557663meiboqu@163.com.
Objective:
To explore the underlying mechanism of ncRNA (MIR22HG) in thyroid papillary carcinomas.
Patients And Methods:
40 pairs of thyroid papillary carcinomas tissues and adjacent normal tissues were collected from patients of the First Affiliated Hospital of Guangxi Medical University, who underwent oral surgery. qRT-PCR was applied to detect the expression of MIR22HG, miR-24-3p and p27kip1 in tissues and cells. Western blot was used to measure the protein level of p27kip1 in tissues and cells. Kaplan-Meier plot was used to analyze the overall survival rates in thyroid papillary carcinomas. Pearson's correlation analysis was used to analyze the correlation relationship among MIR22HG, miR-24-3p and p27kip1 expression. Flow cytometric assay was applied to measure cell apoptosis. Transwell assay was used to assess cell migration and invasion abilities. Luciferase reporter assay was applied to verify the molecular relationships among MIR22HG, miR-24-3p and p27kip1 in thyroid papillary carcinomas.
Results:
LncRNA MIR22HG and p27kip expressed low while miR-24-3p expressed high in thyroid papillary carcinomas and cells. Overexpression of MIR22HG inhibited cell proliferation, migration and invasion, whereas promoted cell apoptosis in thyroid papillary carcinomas cells. However, these effects were reversed by upregulation of miR-24-3p. Further exploration showed that the promoted effects of miR-24-3p mimics on thyroid papillary carcinomas cells were suppressed by enhancing p27kip1 expression. Meanwhile, MIR22HG induced p27kip1 expression by binding miR-24-3p in thyroid papillary carcinomas.
Conclusions:
MIR22HG inhibited cell growth through modulating p27kip1 by decreasing miR-24-3p expression in thyroid papillary carcinomas, providing a new modulate mechanism and therapeutic targets in thyroid papillary carcinomas.
Insights
Long non-coding RNA MIR22HG inhibits thyroid papillary carcinoma growth by downregulating miR-24-3p, thereby increasing p27kip1 expression. This provides a novel therapeutic target for thyroid cancer.
Area of Science:
- Molecular Oncology
- Non-coding RNA Research
- Thyroid Cancer Biology
Background:
- Thyroid papillary carcinoma is the most common type of thyroid cancer.
- The role of non-coding RNAs (ncRNAs) in cancer development is increasingly recognized.
- Understanding the molecular mechanisms underlying thyroid cancer is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the functional role and underlying mechanism of the ncRNA MIR22HG in thyroid papillary carcinomas.
- To explore the relationship between MIR22HG, miR-24-3p, and p27kip1 in thyroid cancer.
Main Methods:
- Analysis of 40 pairs of thyroid papillary carcinoma and adjacent normal tissues.
- Quantitative real-time PCR (qRT-PCR) and Western blot to assess gene and protein expression.
- Cellular assays including apoptosis, migration, and invasion assays.
- Luciferase reporter assay to confirm molecular interactions.
Main Results:
- MIR22HG and p27kip1 expression were downregulated, while miR-24-3p was upregulated in thyroid papillary carcinomas.
- MIR22HG overexpression inhibited proliferation, migration, and invasion, and promoted apoptosis.
- MIR22HG exerted its tumor-suppressive effects by decreasing miR-24-3p and subsequently increasing p27kip1 expression.
Conclusions:
- MIR22HG acts as a tumor suppressor in thyroid papillary carcinomas.
- The MIR22HG/miR-24-3p/p27kip1 axis represents a novel regulatory mechanism in thyroid cancer.
- MIR22HG modulation offers potential therapeutic strategies for thyroid papillary carcinomas.
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