Growth inhibitory effect of 4-hydroxy-tamoxifen on the BT-20 mammary cancer cell line

1988 ◽  
Vol 31 (4) ◽  
pp. 655-663 ◽  
Author(s):  
C. Chouvet ◽  
E. Vicard ◽  
L. Frappart ◽  
N. Falette ◽  
M.F. Lefebvre ◽  
...  
Keyword(s):  
Cell Line ◽  
Cancer Cell ◽  
Mammary Cancer ◽  
Cancer Cell Line ◽  
Inhibitory Effect ◽  
Growth Inhibitory Effect ◽  
Mammary Cancer Cell ◽  
Growth Inhibitory ◽  
Mammary Cancer Cell Line

Characterization of Non-Adherent Cells from IPC-366, A Canine Inflammatory Mammary Cancer Cell Line

2017 ◽  
Vol 156 (1) ◽  
pp. 120
Author(s):  
S. Caceres ◽  
L. Peña ◽  
L. Lacerda ◽  
M.J. Illera ◽  
R.A. Larson ◽  
...  
Keyword(s):  
Cell Line ◽  
Cancer Cell ◽  
Mammary Cancer ◽  
Cancer Cell Line ◽  
Adherent Cells ◽  
Mammary Cancer Cell ◽  
Mammary Cancer Cell Line

Melatonin Treatment Combined with TGF-β Silencing Inhibits Epithelial- Mesenchymal Transition in CF41 Canine Mammary Cancer Cell Line

2020 ◽  
Vol 20 (8) ◽  
pp. 989-997
Author(s):  
Paulo R. Custódio ◽  
Jucimara Colombo ◽  
Fabrício V. Ventura ◽  
Tialfi B. Castro ◽  
Debora A.P.C. Zuccari
Keyword(s):  
Cell Line ◽  
Cancer Cell ◽  
Mammary Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Cell Line ◽  
Mesenchymal Transition ◽  
Mammary Cancer Cell ◽  
Canine Mammary Cancer ◽  
Mammary Cancer Cell Line ◽  
Tgf Β1

Background: Mammary cancer is the most prevalent type of cancer in female dogs. The main cause of mortality is the occurrence of metastasis. The metastatic process is complex and involves the Epithelial- Mesenchymal Transition (EMT), which can be activated by Transforming Growth Factor beta (TGF-β) and involves changes in cellular phenotype, as well as, in the expression of proteins such as E-cadherin, N-cadherin, vimentin and claudin-7. Melatonin is a hormone with oncostatic and anti-metastatic properties and appears to participate in the TGF-β pathway. Thus, the present work aimed to evaluate the expression of EMT markers, E-cadherin, N-cadherin, vimentin and claudin-7, as well as, the cell migration of the canine mammary cancer cell line, CF41, after treatment with melatonin and TGF-β silencing. Methods: Canine mammary cancer cell line, CF41, was cultured and characterized in relation to markers ER, PR and HER2. Cell line CF41 with reducing expression level of TGF-βwas performed according to Leonel et al. (2017). Expression of the protein E-caderin, N-cadherin, vimentin and claudin-7 was evaluated by immunocytochemistry and quantified by optical densitometry. The analysis of cell migration was performed in transwell chambers with 8μM pore size membrane. Results: CF41 cells present a triple negative phenotype, which is an aggressive phenotype. Immunocytochemistry staining showed increased expression of E-caderin and claudin-7 (P˂0.05) and decreased expression of N-cadherin and vimentin (P˂0.05) in CF41 cells after treatment with 1mM melatonin and TGF-β silencing. Moreover, treatment with melatonin and TGF-β silencing was able to reduce migration in cell line CF41 (P˂0.05). Conclusion: Our data suggests that therapies combining TGF- β1 silencing and melatonin may be effective in suppressing the process of EMT, corroborating the hypothesis that melatonin acts on the TGF-β1 pathway and can reduce the metastatic potential of CF41 cells. This is so far the first study that reports melatonin treatment in CF41 cells with TGF-β1 silencing and its effect on EMT. Thus, further studies are needed to confirm this hypothesis.

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