DNA strand intertwined with thyroid gland silhouette, highlighting methylation markers on genes.

Unlocking Thyroid Health: How DNA Methylation Impacts Gene Expression

"New research reveals the critical role of DNA methylation in regulating miR-21 and miR-146b, key players in papillary thyroid carcinoma."


Thyroid cancer incidence is on the rise, making understanding its underlying mechanisms crucial. One area of increasing interest is how DNA methylation, a process that can alter gene expression, contributes to the development and progression of papillary thyroid carcinoma (PTC), the most common type of thyroid cancer. While genetic mutations have been well-studied, epigenetic modifications like DNA methylation offer another layer of complexity.

A recent study published in Clinical Epigenetics sheds light on the specific role of DNA methylation in regulating microRNAs (miRNAs), small molecules that control gene expression. The researchers focused on how methylation affects the expression of miR-21 and miR-146b, two miRNAs implicated in PTC. By examining the relationship between DNA methylation patterns and miRNA expression, they aimed to uncover potential diagnostic markers and therapeutic targets.

This article explores the findings of this research, translating complex scientific concepts into accessible information for individuals interested in thyroid health, potential biomarkers, and innovative treatment strategies. We'll delve into how DNA methylation impacts miR-21 and miR-146b expression, and what this means for the diagnosis and treatment of PTC.

The Methylation Connection: How It Changes miRNA Expression

DNA strand intertwined with thyroid gland silhouette, highlighting methylation markers on genes.

DNA methylation is a process where a methyl group is added to a DNA molecule. This addition can change the activity of a DNA segment without changing the sequence itself. Think of it as a switch that can turn genes on or off. In the context of cancer, aberrant DNA methylation patterns can lead to the dysregulation of genes involved in cell growth, differentiation, and apoptosis (programmed cell death).

The study revealed that in PTC, the genes encoding miR-21 and miR-146b are hypomethylated, meaning they have fewer methyl groups attached to them compared to normal thyroid tissue. This hypomethylation leads to increased expression of these miRNAs. To confirm their findings, the researchers used a variety of techniques, including:

  • Global Methylation Analysis: A comprehensive screen to identify differentially methylated miRNA-encoding genes.
  • Integrative Analysis (TCGA database): Examining data from The Cancer Genome Atlas (TCGA) to validate initial findings.
  • Data Confirmation: Using pyrosequencing and RT-qPCR to confirm methylation and expression patterns in an independent sample set.
  • Functional Assays: Conducting experiments in PTC cell lines to assess the functional consequences of methylation changes.
The convergence of these methods provided strong evidence that loss of DNA methylation is linked to increased miR-21 and miR-146b expression in PTC. Further analysis revealed that increased levels of these miRNAs were associated with the down-expression of several target messenger RNAs (mRNAs), suggesting that these miRNAs are indeed actively disrupting normal gene regulation.

A New Era for Thyroid Cancer Diagnostics and Therapies?

The study's findings highlight the potential of miR-21 and miR-146b as diagnostic biomarkers for PTC. The researchers found that combining methylation and expression levels of these miRNAs could effectively discriminate between malignant and benign thyroid lesions, with high sensitivity and specificity.

Moreover, the identification of specific mRNA targets regulated by these miRNAs opens avenues for developing targeted therapies. By understanding how these miRNAs contribute to the development and progression of PTC, researchers can explore strategies to inhibit their activity or restore the expression of their target genes.

While further research is needed to translate these findings into clinical applications, this study provides valuable insights into the role of DNA methylation in thyroid cancer. It underscores the importance of epigenetic modifications in cancer development and offers hope for more effective diagnostic and therapeutic approaches in the future.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1186/s13148-018-0579-8, Alternate LINK

Title: Loss Of Dna Methylation Is Related To Increased Expression Of Mir-21 And Mir-146B In Papillary Thyroid Carcinoma

Subject: Genetics (clinical)

Journal: Clinical Epigenetics

Publisher: Springer Science and Business Media LLC

Authors: Isabella Maria Dias Payão Ortiz, Mateus Camargo Barros-Filho, Mariana Bisarro Dos Reis, Caroline Moraes Beltrami, Fabio Albuquerque Marchi, Hellen Kuasne, Luísa Matos Do Canto, Julia Bette Homem De Mello, Cecilie Abildgaard, Clóvis Antônio Lopes Pinto, Luiz Paulo Kowalski, Silvia Regina Rogatto

Published: 2018-11-20

Everything You Need To Know

1

What is DNA methylation?

DNA methylation is a process where a methyl group is added to a DNA molecule. This process can change the activity of a DNA segment without altering its sequence. It acts like a switch, turning genes on or off. In the context of papillary thyroid carcinoma (PTC), aberrant DNA methylation patterns can lead to the dysregulation of genes involved in cell growth, differentiation, and apoptosis (programmed cell death).

2

How does DNA methylation impact miR-21 and miR-146b?

In papillary thyroid carcinoma (PTC), the genes encoding miR-21 and miR-146b are hypomethylated, meaning they have fewer methyl groups attached compared to normal thyroid tissue. This hypomethylation results in increased expression of these miRNAs. This suggests that the loss of DNA methylation is linked to increased miR-21 and miR-146b expression in PTC. This altered expression has implications for the diagnosis and treatment of PTC.

3

What are miR-21 and miR-146b?

miR-21 and miR-146b are microRNAs (miRNAs), small molecules that control gene expression. The research focused on how DNA methylation affects the expression of these miRNAs in papillary thyroid carcinoma (PTC). Increased levels of these miRNAs were associated with the down-expression of several target messenger RNAs (mRNAs), suggesting that these miRNAs are disrupting normal gene regulation.

4

What is the significance of these findings for the diagnosis of thyroid cancer?

The study's findings suggest that miR-21 and miR-146b could be used as diagnostic biomarkers for papillary thyroid carcinoma (PTC). Combining methylation and expression levels of these miRNAs could effectively distinguish between malignant and benign thyroid lesions, with high sensitivity and specificity. This is significant because it offers potential for more accurate and earlier diagnosis of PTC.

5

What are the implications of this research?

The implications include potential for new diagnostic tools and targeted therapies for papillary thyroid carcinoma (PTC). The discovery of the role of DNA methylation in regulating miR-21 and miR-146b could lead to the development of new ways to diagnose PTC, as well as new treatment strategies. The findings highlight the complexity of cancer development and the importance of understanding epigenetic modifications like DNA methylation.

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