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Updated: Feb 28, 2026
07:01
An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
Published on: April 17, 2013
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Acetate Metabolism in Thyroid Cancer Progression
Enke Baldini1, Silvia Cardarelli1, Eleonora Lori1
1Department of Surgery, "Sapienza" University of Rome, 00185 Rome, Italy.
International Journal of Molecular Sciences
|February 27, 2026
Summary
Thyroid cancer cells can use acetate for energy. This study found key acetate metabolism genes are downregulated in papillary thyroid cancers (PTCs), especially in aggressive forms, suggesting new therapeutic targets.
Area of Science:
- Biochemistry
- Oncology
- Molecular Biology
Background:
- Malignant cells exhibit metabolic plasticity, utilizing alternative substrates like acetate instead of glucose.
- Acetate metabolism is increasingly recognized as a potential hallmark of cancer, influencing tumor growth and progression.
Purpose of the Study:
- To investigate the gene expression patterns of acetate metabolism in thyroid carcinomas.
- To correlate these expression profiles with clinical and molecular features of papillary thyroid cancers (PTCs).
Main Methods:
- Analysis of The Cancer Genome Atlas (TCGA) data for 496 PTCs and 59 normal thyroid tissues.
- Real-time RT-PCR validation on 57 PTCs, matched normal tissues, and six anaplastic thyroid carcinomas (ATCs).
Main Results:
- Downregulation of ACSS1, ACSS2, ACACB, PDHA1, SLC16A3, and SLC16A7 genes observed in PTCs compared to normal tissues.
- Significantly lower expression of these genes in BRAF-mutated, tall cell variant, larger, and/or metastatic PTCs.
- Upregulation of ACSS2 in ATCs, indicating metabolic adaptation in aggressive cancers.
Conclusions:
- Thyroid carcinomas display dysregulated acetate metabolism gene expression, particularly reduced mitochondrial oxidative pathways in advanced disease.
- Altered acetate metabolism pathways represent a potential target for novel therapeutic strategies in thyroid cancer treatment.
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