Expression of Smad4 and Smad7 in human thyroid follicular carcinoma cell lines

2003 ◽  
Vol 26 (6) ◽  
pp. 516-521 ◽  
Author(s):  
J. M. Cerutti ◽  
K. N. Ebina ◽  
S. E. Matsuo ◽  
L. Martins ◽  
R. M. B. Maciel ◽  
...  
Keyword(s):  
Cell Lines ◽  
Carcinoma Cell ◽  
Follicular Carcinoma ◽  
Human Thyroid ◽  
Carcinoma Cell Lines ◽  
Thyroid Follicular Carcinoma

scholarly journals Ligands for Peroxisome Proliferator-Activated Receptor γ Inhibit Growth and Induce Apoptosis of Human Papillary Thyroid Carcinoma Cells

2001 ◽  
Vol 86 (5) ◽  
pp. 2170-2177 ◽  
Author(s):  
Kazuyasu Ohta ◽  
Toyoshi Endo ◽  
Kazutaka Haraguchi ◽  
Jerome M. Hershman ◽  
Toshimasa Onaya
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Carcinoma Cells ◽  
Human Thyroid ◽  
Peroxisome Proliferator ◽  
Papillary Thyroid ◽  
Peroxisome Proliferator Activated Receptor ◽  
Carcinoma Cell Lines

Ligands for peroxisome proliferator-activated receptor γ (PPARγ) induce apoptosis and exert antiproliferative effects on several carcinoma cell lines. The present study investigates the expression of PPARγ and the possibility that agonists for PPARγ also inhibit the growth of human thyroid carcinoma cells. We examined this hypothesis using six cell lines, designated BHP thyroid carcinoma cells, which originated from patients with papillary thyroid carcinoma. RT-PCR analysis revealed that the thyroid carcinoma cell lines BHP2–7, 7–13, 10–3, and 18–21 express PPARγ. More PPARγ was expressed in carcinoma than in adjacent normal thyroid tissue in three of six samples of human papillary carcinoma of the thyroid. PPARγ-positive thyroid carcinoma cells were treated with agonists of PPARγ, troglitazone, BRL 49653, and 15-deoxy-Δ12,14-prostaglandin J2. Troglitazone (10μ mol/L), BRL 49653 (10 μmol/L), and 15-deoxy-Δ12,14-prostaglandin J2 (1 μg/mL) decreased[ 3H]thymidine incorporation and reduced cell number, respectively, in BHP carcinoma cell lines that expressed PPARγ. Under low serum conditions, ligands for PPARγ induced condensation of the nucleus and fragmentation of chromatin into nucleosome ladders. These findings indicate that the death of thyroid carcinoma cells is a form of apoptosis. To investigate the molecular mechanism of the apoptosis, we assessed expression of the apoptosis-regulatory genes bcl-2, bax, and c-myc. Troglitazone significantly increased the expression of c-myc messenger RNA but had no effect on the expression of bcl-2 and bax in thyroid carcinoma cells. These results suggest that, at least in part, the induction of apoptosis in human papillary thyroid carcinoma cells may be due to an increase of c-myc. Troglitazone (500 mg/kg·day) significantly inhibited tumor growth and prevented distant metastasis of BHP18–21 tumors in nude mice in vivo. Taken together, these results suggest that PPARγ agonist inhibit cell growth of some types of human thyroid cancer.

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 Expression analysis of facilitative glucose transporters (GLUTs) in human thyroid carcinoma cell lines and primary tumors

2008 ◽  
Vol 291 (1-2) ◽  
pp. 57-62 ◽  
Author(s):  
Raffaele Ciampi ◽  
Agnese Vivaldi ◽  
Cristina Romei ◽  
Alberto Del Guerra ◽  
Piero Salvadori ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Cell Lines ◽  
Expression Analysis ◽  
Carcinoma Cell ◽  
Glucose Transporters ◽  
Human Thyroid ◽  
Primary Tumors ◽  
Carcinoma Cell Lines ◽  
Thyroid Carcinoma Cell

Ape1/Ref-1 expression and cellular localization in human thyroid carcinoma cell lines

2001 ◽  
Vol 24 (3) ◽  
pp. RC10-RC12 ◽  
Author(s):  
D. Russo ◽  
F. Arturi ◽  
S. Bulotta ◽  
L. Pellizzari ◽  
S. Filetti ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Cell Lines ◽  
Cellular Localization ◽  
Carcinoma Cell ◽  
Human Thyroid ◽  
Carcinoma Cell Lines ◽  
Thyroid Carcinoma Cell

scholarly journals Expression of the neoplastic phenotype by human thyroid carcinoma cell lines requires NFκB p65 protein expression

Oncogene ◽  
1997 ◽  
Vol 15 (16) ◽  
pp. 1987-1994 ◽  
Author(s):  
Roberta Visconti ◽  
Janete Cerutti ◽  
Sabrina Battista ◽  
Monica Fedele ◽  
Francesco Trapasso ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Protein Expression ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Human Thyroid ◽  
Neoplastic Phenotype ◽  
Carcinoma Cell Lines ◽  
Thyroid Carcinoma Cell
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