Inhibitory effects of retinoic acid on invasiveness of human thyroid carcinoma cell lines in vitro

2009 ◽  
Vol 32 (9) ◽  
pp. 731-738 ◽  
Author(s):  
L. Lan ◽  
D. Cui ◽  
Y. Luo ◽  
B. Y. Shi ◽  
L. L. Deng ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Thyroid Carcinoma ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Human Thyroid ◽  
Inhibitory Effects ◽  
Carcinoma Cell Lines ◽  
Thyroid Carcinoma Cell

scholarly journals Human thyroid carcinoma cell lines show different retinoic acid receptor repertoires and retinoid responses

2004 ◽  
pp. 547-556 ◽  
Author(s):  
C Schmutzler ◽  
C Hoang-Vu ◽  
B Ruger ◽  
J Kohrle
Keyword(s):  
Retinoic Acid ◽  
Thyroid Carcinoma ◽  
Mrna Expression ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Human Thyroid ◽  
Type I ◽  
Carcinoma Cell Lines ◽  
Thyroid Carcinoma Cell

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.

scholarly journals Retinoic acid-mediated down-regulation of ENO1/MBP-1 gene products caused decreased invasiveness of the follicular thyroid carcinoma cell lines

2008 ◽  
Vol 42 (3) ◽  
pp. 249-260 ◽  
Author(s):  
Bogusz Trojanowicz ◽  
Anja Winkler ◽  
Kathrin Hammje ◽  
Zhouxun Chen ◽  
Carsten Sekulla ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Thyroid Carcinoma ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Follicular Thyroid Carcinoma ◽  
Human Thyroid ◽  
Gene Products ◽  
Down Regulation ◽  
Carcinoma Cell Lines ◽  
Thyroid Carcinoma Cell

Retinoic acid (RA) acts as an anti-proliferative and redifferentiation agent in the therapy of thyroid carcinoma. Our previous studies demonstrated that pretreatment of follicular thyroid carcinoma cell lines FTC-133 and FTC-238 resulted in decreased in vitro proliferation rates and reduced tumor cell growth of xenotransplants. In addition to the previous results, we found that RA led to decreased vitality and invasiveness of FTC-133 and FTC-238 cells as they reacted with reduction of intracellular ATP levels and number of migrated cells respectively. However, the molecular mechanisms by which RA mediates these effects are not well understood. Two-dimensional (2D) screening of the proteins related to ATP metabolism and western blot analysis revealed α-enolase (ENO1) to be down-regulated in FTC-133 and FTC-238 cells after RA treatment. 2D gel detection and mass spectrometric analysis revealed that ENO1 existed as three separate protein spots of distinct pIs (ENO1–A1–A3). Comparative 2D difference gel electrophoresis analysis of fluorescently labeled protein samples of RA-treated and untreated FTC-133 demonstrated a selective down-regulation of ENO1-A1 which we identified as a phosphoprotein. RA caused the dephosphorylation of ENO1-A1. Both, RA-mediated and specific knock-down of ENO1/MBP-1 resulted in the reduction of MYC oncoprotein, and simultaneously decreased proliferation rates of FTC-133 and FTC-238 cell lines. In summary, the RA-mediated down-regulation of the ENO1 gene products and MYC oncoprotein provides a novel molecular mechanism facilitating the anti-proliferative effect of RA in human thyroid carcinoma cells and suggests new pathways for supportive RA therapies.

scholarly journals In Vitro Identification and Characterization of CD133pos Cancer Stem-Like Cells in Anaplastic Thyroid Carcinoma Cell Lines

PLoS ONE ◽  
2008 ◽  
Vol 3 (10) ◽  
pp. e3544 ◽  
Author(s):  
Giovanni Zito ◽  
Pierina Richiusa ◽  
Alessandra Bommarito ◽  
Elvira Carissimi ◽  
Leonardo Russo ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Anaplastic Thyroid Carcinoma ◽  
Carcinoma Cell Lines ◽  
Identification And Characterization ◽  
Thyroid Carcinoma Cell

Re-differentiation of thyroid carcinoma cell lines treated with 5-Aza-2′-deoxycytidine and retinoic acid

2009 ◽  
Vol 307 (1-2) ◽  
pp. 142-148 ◽  
Author(s):  
A. Vivaldi ◽  
F.Y. Miasaki ◽  
R. Ciampi ◽  
L. Agate ◽  
P. Collecchi ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Thyroid Carcinoma ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Carcinoma Cell Lines ◽  
Thyroid Carcinoma Cell
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