Regulation of tyrosinase mRNA levels in mouse melanoma cell clones by melanocyte-stimulating hormone and cyclic AMP

1989 ◽  
Vol 15 (3) ◽  
pp. 255-263 ◽  
Author(s):  
George E. Hoganson ◽  
Florence Ledwitz-Rigby ◽  
Richard L. Davidson ◽  
Bryan B. Fuller
Keyword(s):  
Cyclic Amp ◽  
Melanoma Cell ◽  
Mrna Levels ◽  
Mouse Melanoma ◽  
Melanocyte Stimulating Hormone ◽  
Mouse Melanoma Cell ◽  
Cell Clones ◽  
Stimulating Hormone

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

5-Bromo-2-deoxyuridine regulates invasiveness and expression of integrins and matrix-degrading proteinases in a differentiated hamster melanoma cell

1993 ◽  
Vol 105 (1) ◽  
pp. 191-201 ◽  
Author(s):  
L. Thomas ◽  
P.W. Chan ◽  
S. Chang ◽  
C. Damsky
Keyword(s):  
Extracellular Matrix ◽  
Tumor Progression ◽  
Melanoma Cell ◽  
Critical Role ◽  
Terminal Differentiation ◽  
Cell System ◽  
Melanocyte Stimulating Hormone ◽  
Complex Processes ◽  
Differentiation Marker ◽  
Stimulating Hormone

Cell interactions with the extracellular matrix play a critical role in regulating complex processes such as terminal differentiation and tumor progression. In these studies we describe a melanoma cell system that should be useful in addressing the regulation of cell-matrix interactions and the roles they play in regulating differentiation and cell invasiveness. CS (suspension)-1 melanoma cells are relatively well differentiated: they are melanotic, responsive to melanocyte-stimulating hormone, and express TA99, a melanosome membrane differentiation marker. Their repertoire of integrin receptors for extracellular matrix ligands is limited; in particular, they lack receptors for vitronectin, accounting for the observation that they are nonadherent when cultured in the presence of serum. CS-1 cells are noninvasive as well, and express low levels of both metalloproteinases and activated plasminogen activators. Treatment of these cells with melanocyte-stimulating hormone causes them to increase melanin production and assume an arborized phenotype, suggesting that it promotes their further differentiation. In contrast, treatment of CS-1 with the thymidine analog 5-bromodeoxyuridine, converts them to a highly invasive cell population (termed BCS-1) that loses its differentiated properties and responsiveness to melanocyte-stimulating hormone, acquires a broad integrin repertoire (including vitronectin receptors), and expresses elevated levels of metalloproteinases and activated urokinase. From these observations and findings of others on BrdU treatment of other developmental lineages, we hypothesize that BrdU both suppresses differentiation and promotes invasiveness of CS-1 cells. The demonstrated manipulability of CS-1 cells should make them extremely useful for studying the regulation of both terminal differentiation and tumor progression in the melanocyte lineage.

scholarly journals Effect of Natural Plant Water Extracts Suppressed Melanin Production in B16 Mouse Melanoma Cell

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Tae Hyuk Kim ◽  
Mi Ja Chung ◽  
Dae Jung Kim ◽  
Jin Kyoun You ◽  
Dong Joo Seo ◽  
...  
Keyword(s):  
Melanoma Cell ◽  
Plant Water ◽  
Melanin Production ◽  
Natural Plant ◽  
Mouse Melanoma ◽  
Water Extracts ◽  
Mouse Melanoma Cell ◽  
B16 Mouse Melanoma

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.

scholarly journals Inhibition by Tyroserleutide (YSL) on the Invasion and Adhesion of the Mouse Melanoma Cell

2007 ◽  
Vol 13 (1-2) ◽  
pp. 14-21 ◽  
Author(s):  
Zhi Yao ◽  
Xu-chun Che ◽  
Rong Lu ◽  
Min-na Zheng ◽  
Zhi-feng Zhu ◽  
...  
Keyword(s):  
Melanoma Cell ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell

scholarly journals Cell surface phosphatidylinositol-anchored heparan sulfate proteoglycan initiates mouse melanoma cell adhesion to a fibronectin-derived, heparin-binding synthetic peptide

1992 ◽  
Vol 117 (6) ◽  
pp. 1331-1341 ◽  
Author(s):  
SL Drake ◽  
DJ Klein ◽  
DJ Mickelson ◽  
TR Oegema ◽  
LT Furcht ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Cell Surface ◽  
Heparan Sulfate ◽  
Melanoma Cell ◽  
Synthetic Peptide ◽  
Core Protein ◽  
Melanoma Cells ◽  
Heparin Binding ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell

Cell surface heparan sulfate proteoglycan (HSPG) from metastatic mouse melanoma cells initiates cell adhesion to the synthetic peptide FN-C/H II, a heparin-binding peptide from the 33-kD A chain-derived fragment of fibronectin. Mouse melanoma cell adhesion to FN-C/H II was sensitive to soluble heparin and pretreatment of mouse melanoma cells with heparitinase. In contrast, cell adhesion to the fibronectin synthetic peptide CS1 is mediated through an alpha 4 beta 1 integrin and was resistant to heparin or heparitinase treatment. Mouse melanoma cell HSPG was metabolically labeled with [35S]sulfate and extracted with detergent. After HPLC-DEAE purification, 35S-HSPG eluted from a dissociative CL-4B column with a Kav approximately 0.45, while 35S-heparan sulfate (HS) chains eluted with a Kav approximately 0.62. The HSPG contained a major 63-kD core protein after heparitinase digestion. Polyclonal antibodies generated against HSPG purified from mouse melanoma cells grown in vivo also identified a 63-kD core protein. This HSPG is an integral plasma membrane component by virtue of its binding to Octyl Sepharose affinity columns and that anti-HSPG antibody staining exhibited a cell surface localization. The HSPG is anchored to the cell surface through phosphatidylinositol (PI) linkages, as evidenced in part by the ability of PI-specific phospholipase C to eliminate binding of the detergent-extracted HSPG to Octyl Sepharose. Furthermore, the mouse melanoma HSPG core protein could be metabolically labeled with 3H-ethanolamine. The involvement of mouse melanoma cell surface HSPG in cell adhesion to fibronectin was also demonstrated by the ability of anti-HSPG antibodies and anti-HSPG IgG Fab monomers to inhibit mouse melanoma cell adhesion to FN-C/H II. 35S-HSPG and 35S-HS bind to FN-C/H II affinity columns and require 0.25 M NaCl for elution. However, heparitinase-treated 125I-labeled HSPG failed to bind FN-C/H II, suggesting that HS, and not HSPG core protein, binds FN-C/H II. These data support the hypothesis that a phosphatidylinositol-anchored HSPG on mouse melanoma cells (MPIHP-63) initiates recognition to FN-C/H II, and implicate PI-associated signal transduction pathways in mediating melanoma cell adhesion to this defined ligand.

scholarly journals Cell cycle regulation by the Wee1 Inhibitor PD0166285, Pyrido [2,3-d] pyimidine, in the B16 mouse melanoma cell line

BMC Cancer ◽  
2006 ◽  
Vol 6 (1) ◽  
Author(s):  
Osamu Hashimoto ◽  
Masako Shinkawa ◽  
Takuji Torimura ◽  
Toru Nakamura ◽  
Karuppaiyah Selvendiran ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Line ◽  
Melanoma Cell ◽  
Cell Cycle Regulation ◽  
Melanoma Cell Line ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell ◽  
B16 Mouse Melanoma ◽  
Cycle Regulation ◽  
Mouse Melanoma Cell Line
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