scholarly journals ABCG2/BCRP gene expression is related to epithelial–mesenchymal transition inducer genes in a papillary thyroid carcinoma cell line (TPC-1)

2014 ◽  
Vol 52 (3) ◽  
pp. 289-300 ◽  
Author(s):  
E Mato ◽  
C González ◽  
A Moral ◽  
J I Pérez ◽  
O Bell ◽  
...  

Tumor malignancy is associated with the epithelial–mesenchymal transition (EMT) process and resistance to chemotherapy. However, little is known about the relationship between the EMT and the multidrug-resistance gene in thyroid tumor progression. We investigated whether the expression of theABCG2/BCRPgene is associated withZEB1and other EMT inducer genes involved in tumor dedifferentiation. We established a subpopulation of cells that express theABCG2/BCRPgene derived from the thyroid papillary carcinoma cell line (TPC-1), the so-called TPC-1 MITO-resistant subline. The most relevant findings in these TPC-1 selected cells were a statistically significant upregulation ofZEB1andTWIST1(35- and 15-fold change respectively), no changes in the relative expression of vimentin andSNAIL1, and no expression of E-cadherin. The TPC-1 MITO-resistant subline displayed a faster migration and greater invasive ability than parental cells in correlation with a significant upregulation of the survivin (BIRC5) gene (twofold change,P<0.05). The knockdown ofZEB1promoted nuclear re-expression of E-cadherin, reduced expression of vimentin, N-cadherin, andBIRC5genes, and reduced cell migration (P<0.05). Analysis of human thyroid carcinoma showed a slight overexpression of theABCG2/BCRPat stages I and II (P<0.01), and a higher overexpression at stages III and IV (P<0.01).SNAIL1,TWIST1, andZEB1genes showed higher expression at stages III and IV than at stages I and II. E- and N-cadherin genes were upregulated at stages I and II of the disease (ninefold and tenfold change, respectively,P<0.01) but downregulated at stages III and IV (fourfold lower,P<0.01). These results could be a promising starting point for further study of the role of theABCG2/BCRPgene in the progression of thyroid tumor.

1992 ◽  
Vol 83 (2) ◽  
pp. 153-158 ◽  
Author(s):  
Kaoru Tohyama ◽  
Yataro Yoshida ◽  
Kensaku Ohashi ◽  
Emiko Sano ◽  
Hisataka Kobayashi ◽  
...  

Human Cell ◽  
2020 ◽  
Vol 33 (3) ◽  
pp. 545-558
Author(s):  
Naoto Tani ◽  
Mayumi Ishikawa ◽  
Miho Watanabe ◽  
Tomoya Ikeda ◽  
Takaki Ishikawa

Abstract This study aimed to investigate the usefulness of the thyroid-related hormones as markers of acute systemic hypoxia/ischemia to identify deaths caused by asphyxiation due to neck compression in human autopsy cases. The following deaths from pathophysiological conditions were examined: mechanical asphyxia and acute/subacute blunt head injury; acute/subacute non-head blunt injury; sharp instrument injury as the hemorrhagic shock condition; drowning as alveolar injury; burn; and death due to cardiac dysfunction. Blood samples were collected from the left and right cardiac chambers and iliac veins, and serum triiodothyronine (T3), thyroxine (T4), thyroglobulin (Tg), and thyroid-stimulating hormone (TSH) levels were measured using electrochemiluminescence immunoassays. Two types of thyroid cell lines were used to confirm independent thyroid function under the condition of hypoxia (3% O2). The human thyroid carcinoma cell line (HOTHC) cell line derived from human anaplastic thyroid carcinoma and the UD-PTC (sample of the second resection papillary thyroid carcinoma) cell line derived from human thyroid papillary adenoma, which forms Tg retention follicles, were used to examine the secretion levels of T3, T4, and Tg hormones. The results showed a strong correlation between T3 and T4 levels in all blood sampling sites, while the TSH and Tg levels were not correlated with the other markers. Serum T3 and T4 levels were higher in cases of mechanical asphyxia and acute/subacute blunt head injury, representing hypoxic and ischemic conditions of the brain as compared to those in other causes of death. In the thyroid gland cell line, T4, T3, and Tg levels were stimulated after exposure to hypoxia for 10–30 min. These findings suggest that systemic advanced hypoxia/ischemia may cause a rapid and TSH-independent release of T3 and T4 thyroid hormones in autopsy cases. These findings demonstrate that increased thyroid-related hormone (T3 and T4) levels in the pathophysiological field may indicate systemic hypoxia/ischemia.


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