Paracrine Effect of Human Chorionic Gonadotropin Ectopically Produced from Papillary Thyroid Cancer Cells on Growth and Function of FRTL-5 Rat Thyroid Cells

Thyroid ◽  
1997 ◽  
Vol 7 (5) ◽  
pp. 779-782 ◽  
Author(s):  
NORIKO SAKAGUCHI ◽  
MASAYOSHI YOSHIMURA ◽  
JEROME M. HERSHMAN ◽  
MITSUSHIGE NISHIKAWA ◽  
MITSUO INADA
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Papillary Thyroid Cancer ◽  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Papillary Thyroid ◽  
Thyroid Cells ◽  
Rat Thyroid ◽  
And Function ◽  
Thyroid Cancer Cells

scholarly journals Phosphoinositide-3-kinase inhibition induces sodium/iodide symporter expression in rat thyroid cells and human papillary thyroid cancer cells

2008 ◽  
Vol 199 (2) ◽  
pp. 243-252 ◽  
Author(s):  
Takahiko Kogai ◽  
Saima Sajid-Crockett ◽  
Lynell S Newmarch ◽  
Yan-Yun Liu ◽  
Gregory A Brent
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Papillary Thyroid Cancer ◽  
Pi3k Pathway ◽  
Papillary Thyroid ◽  
Iodide Uptake ◽  
Thyroid Cells ◽  
Pathway Inhibition ◽  
Rat Thyroid ◽  
Thyroid Cancer Cells

TSH stimulation of sodium iodide symporter (NIS) expression in thyroid cancer promotes radioiodine uptake and is required to deliver an effective treatment dose. Activation of the insulin/phosphoinositide-3-kinase (PI3K) signaling pathway in TSH-stimulated thyroid cells reduces NIS expression at the transcriptional level. We, therefore, investigated the effects of PI3K pathway inhibition on iodide uptake and NIS expression in rat thyroid cell lines and human papillary thyroid cancer cells. A PI3K inhibitor, LY294002, significantly enhanced iodide uptake in two rat thyroid cell lines, FRTL-5 and PCCL3. The induction of Nis mRNA by LY294002 occurred 6 h after treatment, and was abolished by a translation inhibitor, cycloheximide. Expression of the transcription factor, Pax8, which stimulates NIS expression, was significantly increased in PCCL3 cells after LY294002 treatment. Removal of insulin abrogated the stimulatory effects of LY294002 on NIS mRNA and protein expression, but not on iodide uptake. These findings suggest that PI3K pathway inhibition results in post-translational stimulation of NIS. Inhibition of the PI3K pathway also significantly increased iodide uptake (∼3.5-fold) in BHP 2–7 papillary thyroid cancer cells (Ret/PTC1 positive), engineered to constitutively express NIS. Pharmacological inhibition of Akt, a factor stimulated by the PI3K pathway, increased exogenous NIS expression in BHP 2–7 as was seen with LY294002, but not increase the endogenous NIS expression in FRTL-5 cells. PI3K pathway inhibition increases functional NIS expression in rat thyroid cells and some papillary thyroid cancer cells by several mechanisms. PI3K inhibitors have the potential to increase radioiodide accumulation in some differentiated thyroid cancer.

scholarly journals Retraction: Overexpression of PCDH8 inhibits proliferation and invasion, and induces apoptosis in papillary thyroid cancer cells

RSC Advances ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 4163-4163
Author(s):  
Laura Fisher
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Papillary Thyroid Cancer ◽  
Papillary Thyroid ◽  
Thyroid Cancer Cells ◽  
Proliferation And Invasion

Retraction of ‘Overexpression of PCDH8 inhibits proliferation and invasion, and induces apoptosis in papillary thyroid cancer cells’ by Liang Chang et al., RSC Adv., 2018, 8, 18030–18037, DOI: 10.1039/C8RA02291G.

Galectin-3 regulates apoptosis and doxorubicin chemoresistance in papillary thyroid cancer cells

2009 ◽  
Vol 379 (2) ◽  
pp. 626-631 ◽  
Author(s):  
Chi-Iou Lin ◽  
Edward E. Whang ◽  
Michael A. Abramson ◽  
David B. Donner ◽  
Monica M. Bertagnolli ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Papillary Thyroid Cancer ◽  
Papillary Thyroid ◽  
Galectin 3 ◽  
Thyroid Cancer Cells

scholarly journals CITED1 promotes proliferation of papillary thyroid cancer cells via the regulation of p21 and p27

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Hai Li ◽  
Hongyu Guan ◽  
Yan Guo ◽  
Weiwei Liang ◽  
Liehua Liu ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Papillary Thyroid Cancer ◽  
Papillary Thyroid ◽  
Thyroid Cancer Cells

scholarly journals The Expression of Transcription Factors is Different in Papillary Thyroid Cancer Cells during TNF - α induced EMT

2021 ◽  
Vol 12 (9) ◽  
pp. 2777-2786
Author(s):  
Nannan Lv ◽  
Fei Liu ◽  
Lan Cheng ◽  
Feng Liu ◽  
Jinsong Kuang
Keyword(s):  
Transcription Factors ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Papillary Thyroid Cancer ◽  
Papillary Thyroid ◽  
Tnf Α ◽  
Thyroid Cancer Cells

Dual inhibition of BRAF and MEK increases expression of sodium iodide symporter in patient-derived papillary thyroid cancer cells in vitro

Surgery ◽  
2020 ◽  
Vol 167 (1) ◽  
pp. 56-63 ◽  
Author(s):  
Timothy M. Ullmann ◽  
Heng Liang ◽  
Maureen D. Moore ◽  
Isra Al-Jamed ◽  
Katherine D. Gray ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Papillary Thyroid Cancer ◽  
Sodium Iodide ◽  
Papillary Thyroid ◽  
Sodium Iodide Symporter ◽  
Dual Inhibition ◽  
Thyroid Cancer Cells

scholarly journals Dual Oncogenic/Anti-Oncogenic Role of PATZ1 in FRTL5 Rat Thyroid Cells Transformed by the Ha-RasV12 Oncogene

Genes ◽  
2019 ◽  
Vol 10 (2) ◽  
pp. 127 ◽  
Author(s):  
Michela Vitiello ◽  
Giuseppe Palma ◽  
Mario Monaco ◽  
Anna Bello ◽  
Simona Camorani ◽  
...  
Keyword(s):  
Stem Cell ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Tumor Growth Rate ◽  
Stem Cell Markers ◽  
Thyroid Cells ◽  
Mesenchymal Transition ◽  
Rat Thyroid ◽  
The Impact ◽  
Thyroid Cancer Cells

PATZ1 is a transcriptional factor downregulated in thyroid cancer whose re-expression in thyroid cancer cells leads to a partial reversion of the malignant phenotype, including the capacity to proliferate, migrate, and undergo epithelial-to-mesenchymal transition. We have recently shown that PATZ1 is specifically downregulated downstream of the Ras oncogenic signaling through miR-29b, and that restoration of PATZ1 in Ha-Ras transformed FRTL5 rat thyroid cells is able to inhibit their capacities to proliferate and migrate in vitro. Here, we analyzed the impact of PATZ1 expression on the in vivo tumorigenesis of these cells. Surprisingly, FRTL5-Ras-PATZ1 cells showed enhanced tumor initiation when engrafted in nude mice, even if their tumor growth rate was reduced compared to that of FRTL5-Ras control cells. To further investigate the cause of the enhanced tumor engraftment of FRTL5-Ras-PATZ1 cells, we analyzed the stem-like potential of these cells through their capacity to grow as thyrospheres. The results showed that restoration of PATZ1 expression in these cells increases stem cell markers’ expression and self-renewal ability of the thyrospheres while limiting their growth capacity. Therefore, we suggest that PATZ1 may play a role in enhancing the stem cell potential of thyroid cancer cells, but, at the same time, it impairs the proliferation of non-stem cells.

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