scholarly journals Thyroid status modulates T lymphoma growth via cell cycle regulatory proteins and angiogenesis

2014 ◽  
Vol 222 (2) ◽  
pp. 243-255 ◽  
Author(s):  
H A Sterle ◽  
E Valli ◽  
F Cayrol ◽  
M A Paulazo ◽  
D J Martinel Lamas ◽  
...  

We have shownin vitrothat thyroid hormones (THs) regulate the balance between proliferation and apoptosis of T lymphoma cells. The effects of THs on tumor development have been studied, but the results are still controversial. Herein, we show the modulatory action of thyroid status on thein vivogrowth of T lymphoma cells. For this purpose, euthyroid, hypothyroid, and hyperthyroid mice received inoculations of EL4 cells to allow the development of solid tumors. Tumors in the hyperthyroid animals exhibited a higher growth rate, as evidenced by the early appearance of palpable solid tumors and the increased tumor volume. These results are consistent with the rate of cell division determined by staining tumor cells with carboxyfluorescein succinimidyl ester. Additionally, hyperthyroid mice exhibited reduced survival. Hypothyroid mice did not differ significantly from the euthyroid controls with respect to these parameters. Additionally, only tumors from hyperthyroid animals had increased expression levels of proliferating cell nuclear antigen and active caspase 3. Differential expression of cell cycle regulatory proteins was also observed. The levels of cyclins D1 and D3 were augmented in the tumors of the hyperthyroid animals, whereas the cell cycle inhibitors p16/INK4A (CDKN2A) and p27/Kip1 (CDKN1B) and the tumor suppressor p53 (TRP53) were increased in hypothyroid mice. Intratumoral and peritumoral vasculogenesis was increased only in hyperthyroid mice. Therefore, we propose that the thyroid status modulates thein vivogrowth of EL4 T lymphoma through the regulation of cyclin, cyclin-dependent kinase inhibitor, and tumor suppressor gene expression, as well as the stimulation of angiogenesis.

Cell Cycle ◽  
2013 ◽  
Vol 12 (16) ◽  
pp. 2625-2635 ◽  
Author(s):  
Michael K Kullmann ◽  
Claudia Grubbauer ◽  
Katrin Goetsch ◽  
Heidelinde Jäkel ◽  
Silvio R Podmirseg ◽  
...  

2006 ◽  
Vol 85 (1) ◽  
pp. 39-48 ◽  
Author(s):  
Jitka Bartošová ◽  
Kateřina Kuželová ◽  
Michaela Pluskalová ◽  
Iuri Marinov ◽  
Petr Halada ◽  
...  

1993 ◽  
Vol 52 (3) ◽  
pp. 362-372 ◽  
Author(s):  
David A. Brott ◽  
James D. Alvey ◽  
Michael R. Bleavins ◽  
Felix A. de la Iglesia ◽  
Narendra D. Lalwani

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Ruth Guillermo-Lagae ◽  
Sreevidya Santha ◽  
Milton Thomas ◽  
Emily Zoelle ◽  
Jonathan Stevens ◽  
...  

Honokiol, a plant lignan has been shown to have antineoplastic effects against nonmelanoma skin cancer developments in mice. In this study, antineoplastic effects of honokiol were investigated in malignant melanoma models. In vitro effects of honokiol treatment on SKMEL-2 and UACC-62 melanoma cells were evaluated by measuring the cell viability, proliferation, apoptosis, cell cycle analysis, and expressions of various proteins associated with cell cycle progression and apoptosis. For the in vivo study, male nude mice inoculated with SKMEL-2 or UACC-62 cells received injections of sesame oil or honokiol for two to seven weeks. In vitro honokiol treatment caused significant decrease in cell viability, proliferation, cell cycle arrest, increased apoptosis, and modulation of apoptotic and cell cycle regulatory proteins. Honokiol caused an accumulation of cells in the G2/M phase of the cell cycle in SKMEL-2 and G0/G1 phase in UACC-62 cells. An elevated level of caspases and PARP were observed in both cell lines treated with honokiol. A decrease in the expression of various cell cycle regulatory proteins was also observed in honokiol treated cells. Honokiol caused a significant reduction of tumor growth in SKMEL-2 and UACC-62 melanoma xenografts. These findings suggest that honokiol is a good candidate for further studies as a possible treatment for malignant melanoma.


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