scholarly journals Antitumor Effects of Vitamin D Analogs on Hamster and Mouse Melanoma Cell Lines in Relation to Melanin Pigmentation

2015 ◽  
Vol 16 (12) ◽  
pp. 6645-6667 ◽  
Author(s):  
Tomasz Wasiewicz ◽  
Paulina Szyszka ◽  
Miroslawa Cichorek ◽  
Zorica Janjetovic ◽  
Robert Tuckey ◽  
...  
Keyword(s):  
Vitamin D ◽  
Cell Lines ◽  
Melanoma Cell ◽  
Antitumor Effects ◽  
Melanin Pigmentation ◽  
Vitamin D Analogs ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell ◽  
Melanoma Cell Lines

Expression of POMC and MSH-R in human and mouse melanoma cell lines

1995 ◽  
Vol 5 ◽  
pp. 16
Author(s):  
B. Loir ◽  
M-C. Carrière ◽  
G. Ghanem ◽  
J. Drouin ◽  
L. Roselli-Rehfuss
Keyword(s):  
Cell Lines ◽  
Melanoma Cell ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell ◽  
Human And Mouse ◽  
Melanoma Cell Lines

scholarly journals Atorvastatin enhances the antitumor activity of tamoxifen in B16f10 mouse melanoma cell lines

2020 ◽  
Vol 25 (1) ◽  
pp. 83-91
Author(s):  
Maryam Malek ◽  
◽  
Maedeh Ghasemi ◽  
Golnaz Vaseghi ◽  
Ahmad Ghasemi ◽  
...  
Keyword(s):  
Cell Lines ◽  
Melanoma Cell ◽  
Mevalonate Pathway ◽  
Combined Therapy ◽  
Metastatic Malignant Melanoma ◽  
Mouse Melanoma ◽  
Melanoma Cancer ◽  
Mouse Melanoma Cell ◽  
Melanoma Cell Lines

Introduction: Tamoxifen has been used in the treatment of metastatic malignant melanoma more common with other agents in the combined therapy. Up-regulated activity of the mevalonate pathway has been shown in a range of different cancers. Atorvastatin is the most commonly used statin approved for cholesterol reduction by inhibiting the mevalonate pathway and has been shown to inhibit tumor growth. In the present study, we used atorvastatin and tamoxifen combination therapy on B16f10 mouse melanoma cell lines to study whether atorvastatin could increase the sensitivity of melanoma cells to the chemotherapeutic agent such as tamoxifen. Methods: The cell line was treated with different concentrations of tamoxifen and/or atorvastatin for 24 and 48h and the effects of treatment on p53 and RhoA were investigated using quantitative RT-PCR. Results: The combination of atorvastatin and tamoxifen resulted in a potentiation antitumor effect via up-regulation of p53 and down-regulation of RhoA expression against melanoma tumors in vitro. Furthermore, we demonstrated the combination of atorvastatin with tamoxifen could reduce tamoxifen dose to minimize possible detrimental side effects in melanoma. Conclusion: Our results suggested that atorvastatin as a combined therapy with tamoxifen may provide a new approach for improving the efficacy and treating against melanoma cancer but needs further exploration in clinical trials.

Characterization of mouse melanoma cell lines by their mortal malignancy using an experimental metastatic model

Life Sciences ◽  
2002 ◽  
Vol 70 (7) ◽  
pp. 791-798 ◽  
Author(s):  
Kazuki Nakamura ◽  
Noriko Yoshikawa ◽  
Yu Yamaguchi ◽  
Satomi Kagota ◽  
Kazumasa Shinozuka ◽  
...  
Keyword(s):  
Cell Lines ◽  
Melanoma Cell ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell ◽  
Melanoma Cell Lines

Does Melanin Affect the Low LET Radiation Response of Cloudman S91 Mouse Melanoma Cell Lines?

1991 ◽  
Vol 4 (2) ◽  
pp. 80-86 ◽  
Author(s):  
HELENE Z. HILL ◽  
KATHLEEN NELL CATHCART ◽  
JOSEPH BARGELLINI ◽  
ZOLTAN TRIZNA ◽  
GEORGE J. HILL ◽  
...  
Keyword(s):  
Cell Lines ◽  
Melanoma Cell ◽  
Radiation Response ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell ◽  
Melanoma Cell Lines

scholarly journals The YUMM lines: a series of congenic mouse melanoma cell lines with defined genetic alterations

2016 ◽  
Vol 29 (5) ◽  
pp. 590-597 ◽  
Author(s):  
Katrina Meeth ◽  
Jake Xiao Wang ◽  
Goran Micevic ◽  
William Damsky ◽  
Marcus W. Bosenberg
Keyword(s):  
Cell Lines ◽  
Melanoma Cell ◽  
Genetic Alterations ◽  
Congenic Mouse ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell ◽  
Melanoma Cell Lines

scholarly journals NCRs and DNAM-1 mediate NK cell recognition and lysis of human and mouse melanoma cell lines in vitro and in vivo

2009 ◽  
Vol 119 (5) ◽  
pp. 1251-1263 ◽  
Author(s):  
Tadepally Lakshmikanth ◽  
Shannon Burke ◽  
Talib Hassan Ali ◽  
Silvia Kimpfler ◽  
Francesco Ursini ◽  
...  
Keyword(s):  
Cell Lines ◽  
Melanoma Cell ◽  
Nk Cell ◽  
Cell Recognition ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell ◽  
Human And Mouse ◽  
Melanoma Cell Lines

scholarly journals Antiproliferative Activity of Non-Calcemic Vitamin D Analogs on Human Melanoma Lines in Relation to VDR and PDIA3 Receptors

2018 ◽  
Vol 19 (9) ◽  
pp. 2583 ◽  
Author(s):  
Tomasz Wasiewicz ◽  
Anna Piotrowska ◽  
Justyna Wierzbicka ◽  
Andrzej Slominski ◽  
Michal Zmijewski
Keyword(s):  
Vitamin D ◽  
Cell Lines ◽  
Vitamin D Receptor ◽  
Melanoma Cell ◽  
Human Melanoma ◽  
Side Chain ◽  
Short Side ◽  
Vitamin D Analogs ◽  
Splicing Variants ◽  
Melanoma Cell Lines

Vitamin D is a precursor for secosteroidal hormones, which demonstrate pleiotropic biological activities, including the regulation of growth and the differentiation of normal and malignant cells. Our previous studies have indicated that the inhibition of melanoma proliferation by a short side-chain, low calcemic analog of vitamin D—21(OH)pD is not fully dependent on the expression of vitamin D receptor (VDR). We have examined the effects of classic vitamin D metabolites, 1,25(OH)2D3 and 25(OH)D3, and two low calcemic vitamin D analogs, (21(OH)pD and calcipotriol), on proliferation, mRNA expression and vitamin D receptor (VDR) translocation in three human melanoma cell lines: WM98, A375 and SK-MEL-188b (subline b of SK-MEL-188, which lost responsiveness to 1,25(OH)2D3 and became VDR−/−CYP27B1−/−). All tested compounds efficiently inhibited the proliferation of WM98 and A375 melanoma cells except SK-MEL-188b, in which only the short side-chain vitamin D analog—21(OH)pD was effective. Overall, 21(OH)pD was the most potent compound in all three melanoma cell lines in the study. The lack of responsiveness of SK-MEL-188b to 1,25(OH)2D3, 25(OH)D3 and calcipotriol is explained by a lack of characteristic transcripts for the VDR, its splicing variants as well as for vitamin D-activating enzyme CYP27B1. On the other hand, the expression of VDR and its splicing variants and other vitamin D related genes (RXR, PDIA3, CYP3A4, CYP2R1, CYP27B1, CYP24A1 and CYP11A1) was detected in WM98 and A375 melanomas with the transcript levels being modulated by vitamin D analogs. The expression of VDR isoforms in WM98 cells was stimulated strongly by calcipotriol. The antiproliferative activities of 21(OH)pD appear not to require VDR translocation to the nucleus, which explains the high efficacy of this noncalcemic pregnacalciferol analog in SK-MEL-188b melanoma, that is, VDR−/−. Therefore, we propose that 21(OH)pD is a good candidate for melanoma therapy, although the mechanism of its action remains to be defined.

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