scholarly journals Expression of α-Klotho protein in human thyroid cancers — an immunohistochemical study

2019 ◽  
Vol 70 (3) ◽  
pp. 237-240
Author(s):  
Marek Pawlikowski ◽  
Hanna Pisarek ◽  
Magdalena Borkowska ◽  
Katarzyna Winczyk
Endocrinology ◽  
2008 ◽  
Vol 149 (10) ◽  
pp. 5107-5117 ◽  
Author(s):  
Agnès Burniat ◽  
Ling Jin ◽  
Vincent Detours ◽  
Natacha Driessens ◽  
Jean-Christophe Goffard ◽  
...  

We studied gene expression profiles in two mouse models of human thyroid carcinoma: the Tg-RET/PTC3 (RP3) and Tg-E7 mice. RP3 fusion gene is the most frequent mutation found in the first wave post-Chernobyl papillary thyroid cancers (PTCs). E7 is an oncoprotein derived from the human papillomavirus 16 responsible for most cervical carcinoma in women. Both transgenic mice develop thyroid hyperplasia followed by solid differentiated carcinoma in older animals. To understand the different steps leading to carcinoma, we analyzed thyroid gene expression in both strains at different ages by microarray technology. Important biological processes were differentially regulated in the two tumor types. In E7 thyroids, cell cycle was the most up-regulated process, an observation consistent with the huge size of these tumors. In RP3 thyroids, contrary to E7 tumors, several human PTC characteristics were observed: overexpression of many immune-related genes, regulation of human PTC markers, up-regulation of EGF-like growth factors and significant regulation of angiogenesis and extracellular matrix remodeling-related genes. However, similarities were incomplete; they did not concern the overall gene expression and were not conserved in old animals. Therefore, RP3 tumors are partial and transient models of human PTC. They constitute a good model, especially in young animals, to study the respective role of the biological processes shared with human PTC and will allow testing drugs targeting these validated variables.


2021 ◽  
pp. canres.CAN-20-3334-A.2020
Author(s):  
Jeesu Kim ◽  
Byullee Park ◽  
Jeonghoon Ha ◽  
Idan Steinberg ◽  
Sarah M. Hooper ◽  
...  

Author(s):  
Zahra Nozhat ◽  
Maryam Zarkesh ◽  
Enke Baldini ◽  
Samira Mohammadi-Yeganeh ◽  
Feridoun Azizi ◽  
...  

Background: In the last decades, metformin (Met), an herbal anti-diabetic medicine, has been proposed as an anti-cancer agent. Objective: Thyroid cancers are the most common malignancy of the endocrine system. Therefore, the current study was performed to assess the effects of Met on cell proliferation and activation of the Phosphoinositide 3-Kinase (PI3K)/Protein kinase B (AKT)/Forkhead Box O1 (FOXO1) signaling pathway in the Medullary Thyroid Carcinoma (MTC) cells. The effects of Met on the expression of REarranged during Transfection (RET) proto-oncogene were also investigated. Methods: MTC cell line (TT) was treated with 0, 2.5, 5, 10, 20, 30, 40, 50, and 60 mM concentrations of Met for 24, 48, and 72h. The viability and apoptosis of the treated cells were measured by the 3-(4,5-Dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) and Annexin V- Propidium Iodide (PI) assays. The expression level of PI3K, AKT, FOXO1, and RET genes was investigated by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR), and phosphorylation of their proteins was determined by the Enzyme-Linked Immunosorbent Assay (ELISA). Results: Results showed that Met significantly decreased the viability of the MTC cells. Met also reduced the expression level of PI3K, AKT, and FOXO1 genes (P<0.05), whereas it elevated the expression level of RET proto-oncogene (P<0.05). Conclusion : It seems that the Met has cytostatic effect on the TT cells. Our results showed that anti-tumoral effects of Met may be cell type-specific, and according to the induction of RET (as a proto-oncogene) and inhibition of FOXO1 (as a tumor suppressor gene), Met could not be an appropriate agent in treatment of MTC. The antineoplastic activity of Met has been confirmed against several malignancies in "in vitro" and "in vivo" studies. However, its molecular mechanisms in the treatment of different carcinomas particularly in thyroid cancers are not clearly understood and more studies are required to confirm its exact effect on the MTC.


2017 ◽  
Vol 8 (7) ◽  
pp. 3449 ◽  
Author(s):  
Meng Yang ◽  
Lingyi Zhao ◽  
Xujin He ◽  
Na Su ◽  
ChenYang Zhao ◽  
...  

2011 ◽  
Vol 47 (3) ◽  
pp. R91-R103 ◽  
Author(s):  
Dagmara Rusinek ◽  
Sylwia Szpak-Ulczok ◽  
Barbara Jarzab

This review describes the gene expression profile changes associated with the presence of different mutations that contribute to thyroid cell carcinogenesis. The results are discussed in the context of thyroid cancer biology and of the implications for disease prognosis, while the diagnostic aspect has been omitted. For papillary thyroid cancer (PTC), the most characteristic gene expression profile is associated with the presence ofBRAFmutation. BRAF-associated PTC differ profoundly from RET/PTC or RAS-associated cancers. Simultaneously, they retain many characteristic gene expression features common for all PTCs, induced by the alternative mutations activating MAPK pathway. Although the difference between papillary and follicular thyroid cancer (FTC) is significant at the gene expression profile level, surprisingly, the RAS-related signature of FTC is not well specified.PAX8/peroxisome proliferator-activated receptor γ (PPARγ) rearrangements, which occur in FTC as an alternative to theRASmutation, are associated with specific changes in gene expression. Furthermore, the difference between well-differentiated thyroid cancers and poorly differentiated and anaplastic thyroid cancers is mainly a reflection of tumor degree of differentiation and may not be attributed to the presence of characteristic mutations.


1993 ◽  
Vol 96 (5) ◽  
pp. 787-790_1,873 ◽  
Author(s):  
KATSUNARI YANE ◽  
OSAMU TANAKA ◽  
HIROSHI MIYAHARA ◽  
TAKASHI MATSUNAGA ◽  
YOSHITERU KITAHORI ◽  
...  

1978 ◽  
Vol 87 (1) ◽  
pp. 106-113 ◽  
Author(s):  
Colette Thomas-Morvan

ABSTRACT The effect of TSH (50 mU/ml) alone or in combination with theophylline (10 mm) on the cAMP level in human thyroid tissue after a 10 min incubation has been studied in 8 normal tissues, 7 adenomas and 10 thyroid cancers (8 differentiated and 1 anaplastic). Our results have shown the lack of responsiveness to TSH in the 2 anaplastic carcinomas studied, as well as in 4 cases among the 8 differentiated cancers studied. In thyroid adenomas, on the contrary, the cAMP increase in response to TSH was close to that observed in normal tissues. In these adenomas, the mean basal cAMP level (0.43 ± 0.07 pmol/mg tissue) was not statistically different from that in normal tissues (0.36 ± 0.06), while in thyroid cancers the mean basal cAMP level (0.93 ± 0.26) was significantly greater than that in normal tissues (P < 0.05). The cGMP level was measured in the same conditions in 7 normal thyroid tissues and 8 thyroid cancers (7 differentiated and 1 anaplastic). The mean basal cGMP level in these cancers (9 ± 1 fmol/mg tissue) was not statistically different from that in normal tissues (12 ± 2). In response to TSH, no increase of cGMP level was observed in cancers, or in the normal tissues. The disorders of hormone synthesis previously seen in human thyroid cancers did not appear related to a decreased cAMP content, but might be due to a lack of responsiveness to TSH in undifferentiated cancers and in some cases of differentiated carcinomas.


Sign in / Sign up

Export Citation Format

Share Document