Regulatory Single Nucleotide Polymorphism Increases TERT Promoter Activity in Thyroid Carcinoma Cells

Pathobiology ◽  
2020 ◽  
Vol 87 (6) ◽  
pp. 338-344
Author(s):  
Tatsuya Hirokawa ◽  
Yuu Arimasu ◽  
Tomohiro Chiba ◽  
Yoko Nakazato ◽  
Masachika Fujiwara ◽  
...  
Keyword(s):  
Single Nucleotide Polymorphism ◽  
Thyroid Carcinoma ◽  
Cell Lines ◽  
Promoter Activity ◽  
Carcinoma Cell ◽  
Carcinoma Cells ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Carcinoma Cell Lines ◽  
Thyroid Carcinoma Cell

<b><i>Background/Aim:</i></b> The telomerase reverse transcriptase (<i>TERT</i>) promoter has a regulatory single nucleotide polymorphism (rSNP), rs2853669, and occasionally shows point mutations C228T and C250T. Although C228T and C250T have been well examined to increase <i>TERT</i> promoter activity and are known as risk factors for thyroid carcinoma, the significance of rs2853669 has not been well investigated. This study aimed to clarify the influence of rs2853669 on <i>TERT</i> promoter activity in thyroid carcinoma cells. <b><i>Materials:</i></b> Seven of 8 examined thyroid cell lines had rs2853669, 5 had C228T, and 1 had C250T. <b><i>Results:</i></b> Three papillary thyroid carcinoma cell lines, harboring both rs2853669 and C228T, showed higher <i>TERT</i> mRNA expression on real-time PCR than the other cell lines. Anaplastic thyroid carcinoma cell lines, in contrast, showed variable <i>TERT</i> mRNA expression depending on the combination of rs2853669, C228T, and C250T. Luciferase assays, performed to compare the influences of rs2853669, C228T, and C250T on <i>TERT</i> promoter activity in thyroid carcinoma, showed that rs2853669, as well as C228T, increased the promoter activity, and the combination of rs2853669 and C228T increased the promoter activity even more strongly than C228T alone. <b><i>Conclusion:</i></b> We conclude that the presence of rs2853669 within the <i>TERT</i> promoter could be as significant as the C228T mutation in thyroid carcinoma.

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

scholarly journals Differential glycolytic profile and Warburg effect in papillary thyroid carcinoma cell lines

2016 ◽  
Vol 36 (6) ◽  
pp. 3673-3681 ◽  
Author(s):  
Raquel Guimarães Coelho ◽  
Juliana De Menezes Cazarin ◽  
João Paulo Albuquerque Cavalcanti De Albuquerque ◽  
Bruno Moulin De Andrade ◽  
Denise P. Carvalho
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Cell Lines ◽  
Warburg Effect ◽  
Carcinoma Cell ◽  
Papillary Thyroid ◽  
Carcinoma Cell Lines ◽  
Thyroid Carcinoma Cell ◽  
Papillary Thyroid Carcinoma Cell

scholarly journals The Impact of Cysteine-Rich Intestinal Protein 1 (CRIP1) on Thyroid Carcinoma

2017 ◽  
Vol 43 (5) ◽  
pp. 2037-2046 ◽  
Author(s):  
Hong-guang Li ◽  
Li-hong Zhao ◽  
Zhen-hua Zhang ◽  
Jun-zhao Liu ◽  
Ke Ren ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Migration And Invasion ◽  
G1 Arrest ◽  
Prognostic Impact ◽  
Carcinoma Cell Lines ◽  
Intestinal Protein ◽  
The Impact ◽  
Thyroid Carcinoma Cell

Background/Aims: CRIP1 (cysteine-rich intestinal protein 1) has been found in several tumor types; however, its prognostic impact and role in cellular processes, particularly in thyroid carcinoma, are still unclear. Methods: To elucidate the prognostic impact of CRIP1, we analyzed tissues from 58 primary invasive thyroid carcinomas using immunohistochemistry. Western blotting was performed to investigate CRIP1 protein expression in the thyrocyte cell line Nthy-ori 3-1 and four different thyroid carcinoma cell lines, K1, TPC-1, TT, and SW579. Endogenous expression of CRIP1 was suppressed using a siRNA (si-CRIP1). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was used to investigate cell viability. Flow cytometric analysis was used to detect cell cycle progression and cell apoptosis. The effects of silencing CRIP1 on cell migration and invasion were detected using the transwell assay. Results: The immunohistochemistry results showed that CRIP1 was overexpressed in thyroid carcinoma. CRIP1 expression was associated with tumor size, TNM stage, and lymphatic metastasis, but not with age, gender, and tumor location. In addition, the expression of CRIP1 in K1, TPC-1, TT, and SW529 cells was higher than that in the Nthy-ori 3-1 cells. The highest expression was observed in the SW579 and TT cells. Furthermore, silencing CRIP1 inhibited the proliferation, migration, and invasion of thyroid carcinoma cell lines SW579 and TT. We also found that silencing CRIP1 induced G1 arrest and apoptosis of thyroid carcinoma cell lines SW579 and TT. Conclusion: In conclusion, CRIP1 acts as an oncogene in the cell proliferation, migration, and invasion processes of thyroid carcinoma. CRIP1 may serve well as an independent prognostic marker with significant predictive power for use in thyroid carcinoma therapy.

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 Effect of Imatinib Mesylate (Gleevec) on Anaplastic Thyroid Carcinoma Cell Lines 1

2003 ◽  
Vol 88 (10) ◽  
pp. 5043-5044 ◽  
Author(s):  
Constantine S. Mitsiades ◽  
Despoina Sykoutri ◽  
Ciaran McMullan ◽  
Vassiliki Poulaki ◽  
Nicholas Mitsiades
Keyword(s):  
Thyroid Carcinoma ◽  
Imatinib Mesylate ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Anaplastic Thyroid Carcinoma ◽  
Carcinoma Cell Lines ◽  
Thyroid Carcinoma Cell
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