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Updated: May 31, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MiR-1 is a tumor suppressor in thyroid carcinogenesis targeting CCND2, CXCR4, and SDF-1alpha
Vincenza Leone1, Daniela D'Angelo, Ileana Rubio
1Istituto di Endocrinologia ed Oncologia Sperimentale del Consiglio Nazionale delle Ricerche, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Facoltà di Medicina e Chirurgia di Napoli, Università degli Studi di Napoli Federico II, Centro Ingegneria Genetica and European School of Molecular Medicine, 80131 Naples, Italy.
Context:
Micro-RNA have emerged as an important class of short endogenous RNA that act as posttranscriptional regulators of gene expression and are constantly deregulated in human cancer. MiR-1 has been found down-regulated in lung, colon, and prostate cancer.
Objectives:
In this study, we investigated the possible role of miR-1 in thyroid carcinogenesis.
Design:
We have analyzed miR-1 expression in a panel of thyroid neoplasias including benign and malignant lesions and searched for miR-1 targets.
Results:
Our results show that miR-1 expression is drastically down-regulated in thyroid adenomas and carcinomas in comparison with normal thyroid tissue. Interestingly, miR-1 down-regulation was also found in thyroid hyperproliferative nonneoplastic lesions such as goiters. We identified the CCND2, coding for the cyclin D2 (CCND2) protein that favors the G1/S transition, CXCR4, and SDF-1α genes, coding for the receptor for the stromal cell derived factor-1 (SDF-1)/CXCL12 chemokine and its ligand SDF-1/CXCL12, respectively, as miR-1 targets. An inverse correlation was found between miR-1 expression and CXC chemokine receptor 4 (CXCR4) and SDF-1α protein levels in papillary and anaplastic thyroid carcinomas. Consistent with a role of the CCND2 protein in cell proliferation and CXCR4 and SDF-1α proteins in cell invasion and metastasis, functional studies demonstrate that miR-1 is able to inhibit thyroid carcinoma cell proliferation and migration.
Conclusions:
These results indicate the involvement of miR-1 in thyroid cell proliferation and migration, validating a role of miR-1 down-regulation in thyroid carcinogenesis.
Insights
MicroRNA-1 (miR-1) is down-regulated in thyroid tumors, including benign and malignant types. This suggests miR-1 plays a role in thyroid cancer development by affecting cell proliferation and migration.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- MicroRNAs (miRNAs) are key posttranscriptional regulators of gene expression.
- Dysregulation of miRNAs is common in human cancers.
- MiR-1 is notably downregulated in lung, colon, and prostate cancers.
Purpose of the Study:
- To investigate the role of miR-1 in thyroid carcinogenesis.
- To analyze miR-1 expression in various thyroid lesions.
- To identify potential miR-1 targets in thyroid cancer.
Main Methods:
- Analysis of miR-1 expression in benign and malignant thyroid neoplasias.
- Identification of miR-1 target genes using bioinformatics and experimental validation.
- Correlation of miR-1 levels with target protein expression in thyroid carcinomas.
- Functional assays to assess the impact of miR-1 on cancer cell behavior.
Main Results:
- Significant downregulation of miR-1 observed in thyroid adenomas, carcinomas, and even hyperplastic goiters compared to normal thyroid tissue.
- Identified CCND2, CXCR4, and SDF-1α as direct targets of miR-1.
- Inverse correlation between miR-1 expression and CXCR4/SDF-1α protein levels in papillary and anaplastic thyroid carcinomas.
- miR-1 demonstrated the ability to inhibit thyroid carcinoma cell proliferation and migration in vitro.
Conclusions:
- Downregulation of miR-1 is implicated in thyroid carcinogenesis.
- miR-1 plays a crucial role in regulating thyroid cell proliferation and migration.
- Restoring miR-1 levels may represent a therapeutic strategy for thyroid cancer.
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