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Updated: Mar 24, 2026

Spontaneous Murine Model of Anaplastic Thyroid Cancer
Published on: February 3, 2023
MicroRNAs let7 expression in thyroid cancer: correlation with their deputed targets HMGA2 and SLC5A5
Alexander I Damanakis1, Sabine Eckhardt1, Annette Wunderlich1
1Department of Visceral, Thoracic and Vascular Surgery, Philipps University Marburg, Baldingerstrasse, 35043, Marburg, Germany.
Purpose:
Thyroid cancer (TC), the most common endocrine malignancy, increases its incidence worldwide. MicroRNAs have been shown to be abnormally expressed in tumors and could represent valid diagnostic markers for patients affected by TC. Our aim was to analyze the expression of tumorsuppressor hsa-let7b-5p and hsa-let7f-5p, together with their predicted targets SLC5A5 (NIS) and HMGA2, in papillary (PTC), follicular (FTC) and anaplastic (ATC).
Methods:
8 FTC, 14 PTC, 12 ATC and three normal thyroid tissue samples were analyzed for the expression of pre-let7b, hsa-let7b-5p and hsa-let7f-5p as SLC5A5 and HMGA2 by RT-qPCR. Data were analyzed by REST 2008.
Results:
FTC patients showed a significant down-regulation of hsa-let7b-5p and its precursor. hsa-let7f-5p was overexpressed, and SLC5A5 was strongly suppressed. HMGA2 was overexpressed, reflecting no correlation with its regulatory let7 miRNAs. PTC samples were characterized by up-regulation of hsa-let7b-5p, its precursor and hsa-let7f-5p. SLC5A5 was strongly suppressed in comparison with normal thyroid tissue. HMGA2 was overexpressed, as shown in FTC, also. ATC samples showed a similar miRNAs profile as PTC. In contrast with FTC and PTC, these patients showed a stable or up-regulated SLC5A5 and HMGA2.
Conclusions:
Expression of HMGA2 is not correlated with the regulatory let7 miRNAs. Interestingly, SLC5A5 was down-regulated in FTC and PTC. Its expression could be modulated by hsa-let-7f-5p. ATC showed a loss of SLC5A5/hsa-let7f-5p correlation. SLC5A5, in ATC, needs further investigation to clarify the genetic/epigenetic mechanism altering its expression.
Insights
Thyroid cancer microRNA expression varies by type. hsa-let-7b-5p and hsa-let-7f-5p showed distinct patterns, impacting SLC5A5 and HMGA2 in follicular, papillary, and anaplastic thyroid cancers.
Area of Science:
- Endocrinology
- Molecular Biology
- Oncology
Background:
- Thyroid cancer (TC) is the most common endocrine malignancy with increasing incidence.
- MicroRNAs (miRNAs) are implicated in tumorigenesis and can serve as diagnostic markers for TC.
- Specific miRNAs, hsa-let-7b-5p and hsa-let-7f-5p, and their targets SLC5A5 and HMGA2, are investigated for their roles in different TC subtypes.
Purpose of the Study:
- To analyze the expression of tumor suppressor miRNAs hsa-let-7b-5p and hsa-let-7f-5p.
- To investigate the expression of their predicted targets, SLC5A5 (sodium-iodide symporter) and HMGA2 (high mobility group AT-hook 2).
- To compare these expression patterns across papillary (PTC), follicular (FTC), and anaplastic (ATC) thyroid cancer subtypes.
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to measure the expression of pre-let-7b, hsa-let-7b-5p, hsa-let-7f-5p, SLC5A5, and HMGA2.
- Samples included 8 FTC, 14 PTC, 12 ATC, and 3 normal thyroid tissues.
- Data analysis was performed using REST 2008 software.
Main Results:
- Follicular thyroid cancer (FTC) exhibited down-regulation of hsa-let-7b-5p, overexpression of hsa-let-7f-5p, and suppressed SLC5A5, with HMGA2 overexpression.
- Papillary thyroid cancer (PTC) showed up-regulation of hsa-let-7b-5p and hsa-let-7f-5p, suppressed SLC5A5, and overexpressed HMGA2.
- Anaplastic thyroid cancer (ATC) displayed similar miRNA profiles to PTC but with stable or up-regulated SLC5A5 and HMGA2, indicating a loss of correlation.
Conclusions:
- HMGA2 expression is not consistently correlated with regulatory let-7 miRNAs across all thyroid cancer subtypes.
- SLC5A5 was down-regulated in FTC and PTC, potentially modulated by hsa-let-7f-5p.
- ATC presents a distinct pattern with a loss of SLC5A5/hsa-let-7f-5p correlation, warranting further investigation into the mechanisms altering SLC5A5 expression.
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