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Human thyroid carcinoma cell lines show different retinoic acid receptor repertoires and retinoid responses
Cornelia Schmutzler1, Cuong Hoang-Vu, Barbara Rüger
1Institut für Experimentelle Endokrinologie, Charité, Universitätsmedizin Berlin, Germany.
Objective:
Disturbed expression of retinoic acid (RA) receptors (RAR/RXR) contributes to the pathogenesis and tumor progression of epithelial carcinomas.
Design:
To examine whether altered responses to retinoids may correlate with differences in RA receptor equipment, retinoid effects were examined in human thyroid carcinoma cell lines of various differentiation stages in culture and after xenotransplantation onto rodent models.
Methods:
Cell growth was assessed by the MTT test, mRNA expression was examined by Northern blot and quantitative competitive RT-PCR, and type I 5'-deiodinase (5'DI) activity was measured by in vitro deiodination assay. Nude rats and mice were used for xenotransplantation experiments.
Results:
All-trans-RA and RAR-selective synthetic retinoids stimulated activity and mRNA expression of the thyroid differentiation marker 5'DI in the follicular thyroid carcinoma cell line FTC-133. In the less differentiated FTC-238 cells, stimulation of 5'DI activity was less pronounced than in FTC-133 cells, and a reduced level of RAR beta mRNA was detected. In the anaplastic thyroid carcinoma cell lines HTh 74 and C 643, the activity of 5'DI was not increased by retinoids, and expression of RAR alpha mRNA was reduced. Proliferation of FTC-133 and FTC-238 cells was decreased by all-trans-RA. Pretreatment of FTC-133 with RA resulted in a reduced tumor growth in xenotransplantation experiments as compared with untreated control cells. This reduction was less pronounced in the case of FTC-238 cells. Thus, retinoid therapy might be applied to treat follicular thyroid carcinomas. However, tumor-specific RAR repertoires need to be analyzed as a prerequisite for successful intervention with appropriate, probably receptor-selective retinoids.
Insights
Retinoid receptors (RAR/RXR) are crucial in epithelial carcinomas. This study shows retinoid therapy can treat follicular thyroid cancer, but receptor analysis is key for effective treatment.
Area of Science:
- Endocrinology
- Molecular Biology
- Oncology
Background:
- Disturbed retinoic acid (RA) receptor (RAR/RXR) expression is implicated in epithelial carcinoma pathogenesis and progression.
- Understanding retinoid responses in relation to RA receptor profiles is essential for targeted therapies.
Purpose of the Study:
- To investigate the correlation between altered retinoid responses and RA receptor expression in human thyroid carcinoma cell lines.
- To assess the therapeutic potential of retinoids in different stages of thyroid cancer differentiation.
Main Methods:
- Utilized human thyroid carcinoma cell lines (FTC-133, FTC-238, HTh 74, C 643) representing various differentiation stages.
- Assessed cell proliferation (MTT assay), mRNA expression (Northern blot, RT-PCR), and type I 5'-deiodinase (5'DI) activity.
- Conducted xenotransplantation experiments in nude rats and mice to evaluate in vivo tumor growth.
Main Results:
- Retinoids stimulated 5'DI activity and expression in well-differentiated FTC-133 cells, with less effect in FTC-238 cells and no effect in anaplastic lines (HTh 74, C 643).
- Reduced RAR beta mRNA was observed in FTC-238 cells, and reduced RAR alpha mRNA in anaplastic lines.
- All-trans-RA decreased proliferation in FTC-133 and FTC-238 cells and reduced tumor growth in xenografts, particularly in FTC-133.
Conclusions:
- Retinoid therapy shows promise for treating follicular thyroid carcinomas.
- Tailoring retinoid interventions requires prior analysis of tumor-specific RAR repertoires for optimal receptor-selective drug selection.
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