Resistance to ursolic acid-induced apoptosis through involvement of melanogenesis and COX-2/PGE2 pathways in human M4Beu melanoma cancer cells

2016 ◽  
Vol 345 (1) ◽  
pp. 60-69 ◽  
Author(s):  
Lama Hassan ◽  
Aline Pinon ◽  
Youness Limami ◽  
Josiane Seeman ◽  
Chloe Fidanzi-Dugas ◽  
...  
Biochimie ◽  
2012 ◽  
Vol 94 (8) ◽  
pp. 1754-1763 ◽  
Author(s):  
Youness Limami ◽  
Aline Pinon ◽  
David Yannick Leger ◽  
Emilie Pinault ◽  
Christiane Delage ◽  
...  

1998 ◽  
Vol 274 (6) ◽  
pp. G1061-G1067 ◽  
Author(s):  
Hitoshi Sawaoka ◽  
Sunao Kawano ◽  
Shingo Tsuji ◽  
Masahiko Tsujii ◽  
Edhi S. Gunawan ◽  
...  

To clarify the role of mitogen-inducible cyclooxygenase (COX-2) in the development of malignant tumors, we investigated the effects of COX-2 inhibitors on the growth of gastric cancer xenografts in nude mice in vivo. MKN45 gastric cancer cells (5 × 106cells/animal) that overexpress COX-2 were inoculated subcutaneously into athymic mice. NS-398, a specific COX-2 inhibitor, or indomethacin, a nonspecific COX-2 inhibitor, was administered orally to animals every day for 20 days. These drugs reduced the tumor volume significantly. Immunohistochemistry using bromodeoxyuridine, nick end labeling, and electron microscopy showed that NS-398 induced apoptosis in cancer cells in a dose-dependent manner and inhibited cancer cell replication slightly. Indomethacin also induced apoptosis and suppressed replication of tumor cells. There was a significant negative correlation between tumor volume and apoptotic cell number within the tumor. These results are consistent with the hypothesis that COX-2 inhibitors suppress growth of gastric cancer xenografts mainly by inducing apoptosis and suppressing replication of the neoplastic cells. It follows that COX-2 plays an important role in the development of gastric cancer.


2016 ◽  
Vol 117 (12) ◽  
pp. 2875-2885 ◽  
Author(s):  
Josiane Semaan ◽  
Aline Pinon ◽  
Benjamin Rioux ◽  
Lama Hassan ◽  
Youness Limami ◽  
...  

2003 ◽  
Vol 88 (3) ◽  
pp. 429-433 ◽  
Author(s):  
A.R Munkarah ◽  
Z Genhai ◽  
R Morris ◽  
V.V Baker ◽  
G Deppe ◽  
...  

2007 ◽  
Vol 9 (4) ◽  
Author(s):  
Takeshi Sugimoto ◽  
Chandra Bartholomeusz ◽  
Ana M Tari ◽  
Naoto T Ueno

2018 ◽  
Vol 44 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Ozge Cevik ◽  
Fatma Aysun Turut ◽  
Hilal Acidereli ◽  
Sahin Yildirim

Abstract Background Potential targets for prostate cancer therapy are urgently needed for curative of patients. Cyclosporine-A (CsA), an immunosuppressive and a selective cyclooxygenase-2 (COX-2) inhibitor, exerts antitumor activity. However, the molecular effects of CsA is not fully understood in prostate cancer. In this research, we sought to determine role and mechanism of CsA in prostate cancer. Materials and methods PC3 and DU145 cells were treated with CsA time (12, 24, 48 h) and dose dependent (2.5, 10, 25 μM) and cell survival, migration, colony formation, expression of apoptosis related proteins/genes using MTT assay, scratch assay, Western blotting/qPCR. At the same time, cells treated with CsA to test on the effects of COX-2 promoter activity using luciferase reporter plasmid. Lastly, functional role in the CsA treatment prostate cancer cells were interrogated for relationship of TGFβ, Akt, caspases and COX-2. Results These study findings provided direct evidences that the CsA induced apoptosis and downregulated migration. Conclusions CsA downregulated Akt as well as COX-2 and upregulated TGFβ, resulting in the suppression of cell migration which was augmented a potential therapeutic of CsA in prostate cancer cells.


2013 ◽  
Vol 65 (5) ◽  
pp. 1366-1374 ◽  
Author(s):  
Ji-Hyuk Park ◽  
Hee-Young Kwon ◽  
Eun Jung Sohn ◽  
Kyung A. Kim ◽  
Bonglee Kim ◽  
...  

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