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Updated: Jun 12, 2026

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
Published on: April 17, 2013
Proteomic approach reveals novel targets for retinoic acid-mediated therapy of thyroid carcinoma
Bogusz Trojanowicz1, Carsten Sekulla, Kerstin Lorenz
1Universitätsklinik und Poliklinik für Allgemein-, Viszeral- und Gefässchirurgie, Martin-Luther Universität, 06097 Halle, Germany.
Abstract:
Our previous studies demonstrated that retinoic acid (RA)-induced reduction of both, the key glycolytic enzyme ENO1 and proliferation-promoting c-Myc, resulted in decreased vitality and invasiveness of the follicular thyroid carcinoma cell lines FTC-133 and FTC-238. By employing two-dimensional electrophoresis and mass spectrometry, we identified proteins affected by RA treatment. In addition to previously reported decrease in ENO1 expression, we found that RA led to significantly reduced levels of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), pyruvate kinase isoenzymes M1/M2 (PKM1/M2), peptidyl-prolyl cis-trans isomerase A (PPIA), transketolase (TKT), annexin A2 (ANXA2), glutathione S-transferase P (GSTP1) and peroxiredoxin 2 (PRDX2) as compared to untreated control. The same proteins investigated on thyroid tissues were found to be significantly up-regulated in follicular, papillary and undifferentiated thyroid carcinomas when compared with goiter and adenoma tissues. These findings identify new target proteins for RA-mediated anti-tumor and re-differentiation therapies and provide novel insights into treatments for thyroid carcinoma.
Insights
Retinoic acid (RA) reduces key proteins like ENO1 and GAPDH, decreasing thyroid cancer cell vitality. These proteins are elevated in thyroid tumors, suggesting new therapeutic targets for RA treatment.
Area of Science:
- Oncology
- Biochemistry
- Molecular Biology
Background:
- Retinoic acid (RA) previously reduced ENO1 and c-Myc, decreasing thyroid cancer cell invasiveness.
- Understanding RA's broader molecular effects is crucial for thyroid cancer therapy.
Purpose of the Study:
- To identify proteins affected by RA treatment in follicular thyroid carcinoma cells.
- To investigate the expression of these proteins in various thyroid carcinoma tissues.
Main Methods:
- Two-dimensional electrophoresis and mass spectrometry were used to identify RA-affected proteins.
- Quantitative analysis of specific protein levels in cell lines and thyroid tissues.
Main Results:
- RA significantly reduced ENO1, GAPDH, PKM1/M2, PPIA, TKT, ANXA2, GSTP1, and PRDX2 in thyroid cancer cells.
- These proteins were significantly upregulated in follicular, papillary, and undifferentiated thyroid carcinomas compared to benign thyroid tissues.
Conclusions:
- RA targets multiple glycolytic and cellular stress proteins, impacting thyroid cancer cell behavior.
- Identified proteins represent potential therapeutic targets for RA-mediated anti-tumor and re-differentiation strategies in thyroid carcinoma.
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