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Updated: Aug 12, 2026
An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
Published on: April 17, 2013
Malignant transformation of thyroid follicular cells by galectin-3
Yukinori Takenaka1, Hidenori Inohara, Tadashi Yoshii
1Department of Otolaryngology and Sensory Organ Surgery, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Abstract:
Galectin-3, a beta-galactoside binding lectin, is highly expressed in thyroid carcinomas of follicular cell origin, whereas neither benign thyroid adenomas nor normal thyroid tissues express galectin-3. We previously showed that antisense inhibition of galectin-3 expression markedly reduced the malignant phenotype of thyroid papillary carcinoma cells. In the present study we transfected galectin-3 cDNA into TAD-2 normal thyroid follicular cells. Stable transfectants expressing galectin-3 acquired the phenotype of serum-independent growth, clonogenicity in soft agar, as well as loss of contact inhibition. We also compared the gene expression profile of the galectin-3 transfectants to that of the vehicle control, which revealed that a series of genes were differentially expressed between the two. They include proliferating cell nuclear antigen, replication factor C, and retinoblastoma genes that participate in G1-S transition. These results indicate the transformation of thyroid follicular cells by galectin-3 and possible involvement of galectin-3 in cell cycle.
Insights
Galectin-3 transforms normal thyroid cells into a malignant phenotype, promoting serum-independent growth and altering cell cycle genes. This suggests galectin-3’s role in thyroid cancer development.
Area of Science:
- Molecular Biology
- Oncology
- Cell Biology
Background:
- Galectin-3 is highly expressed in thyroid carcinomas but not in normal or benign thyroid tissues.
- Previous studies demonstrated that inhibiting galectin-3 reduces the malignant phenotype of thyroid papillary carcinoma cells.
Purpose of the Study:
- To investigate the functional role of galectin-3 in normal thyroid follicular cells.
- To determine if galectin-3 expression can induce cellular transformation.
Main Methods:
- Transfection of galectin-3 cDNA into normal thyroid follicular cells (TAD-2).
- Assessment of phenotypic changes including serum-independent growth, clonogenicity in soft agar, and contact inhibition.
- Comparison of gene expression profiles between galectin-3 transfectants and control cells using microarray analysis.
Main Results:
- Stable transfectants expressing galectin-3 exhibited serum-independent growth, formed colonies in soft agar, and lost contact inhibition.
- Gene expression profiling revealed differential expression of genes involved in G1-S cell cycle transition, such as proliferating cell nuclear antigen (PCNA), replication factor C (RFC), and retinoblastoma (Rb) genes.
- These findings indicate that galectin-3 expression induces a transformed phenotype in normal thyroid follicular cells.
Conclusions:
- Galectin-3 expression can transform normal thyroid follicular cells, conferring a malignant phenotype.
- Galectin-3 may play a significant role in thyroid cancer development and progression, potentially through its involvement in cell cycle regulation.
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