Hyposmotically-Activated Efflux of L-Carnitine from a Human Mammary Cancer Cell Line

2001 ◽  
Vol 21 (6) ◽  
pp. 779-787
Author(s):  
D.B. Shennan

Cell-swelling, induced by a hyposmotic challenge, stimulated the efflux of L-carnitine from a human mammary cancer cell line, MDA-MB-231. The response was dependent upon the extent of the osmotic shock. Hyposmotically-activated L-carnitine efflux was inhibited by the anion transport blocker diiodosalicylate. The efflux of taurine from MDA-MB-231 cells was also stimulated by a hyposmotic shock via a pathway sensitive to diiodosalicylate. L-carnitine efflux from MDA-MB-231 cells was stimulated by isosmotic swelling in a manner which was inhibited by diiodosalicylate. The results suggest that L-carnitine may exit cells via a volume-sensitive pathway: it is possible that L-carnitine efflux may utilize the same pathway as amino acids. The efflux of L-carnitine via this route could have a major effect on the intracellular concentration of L-carnitine and could facilitate transepithelial L-carnitine transport.

1988 ◽  
Vol 31 (4) ◽  
pp. 655-663 ◽  
Author(s):  
C. Chouvet ◽  
E. Vicard ◽  
L. Frappart ◽  
N. Falette ◽  
M.F. Lefebvre ◽  
...  

2017 ◽  
Vol 156 (1) ◽  
pp. 120
Author(s):  
S. Caceres ◽  
L. Peña ◽  
L. Lacerda ◽  
M.J. Illera ◽  
R.A. Larson ◽  
...  

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

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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