Elucidation of the effect of plumbagin on the metastatic potential of B16F10 murine melanoma cells via MAPK signalling pathway
Melanoma is the most dangerous form of skin cancer with a very poor prognosis. Melanoma develops when unrepaired DNA damage causes to skin cells to multiply and form malignant tumors. The current therapy is limited by the highly ability of this disease to metastasize rapidly. Plumbagin is a naphthoq...
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Published in | Experimental dermatology Vol. 29; no. 4; pp. 427 - 435 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Denmark
Wiley Subscription Services, Inc
01.04.2020
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Subjects | |
Online Access | Get full text |
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Summary: | Melanoma is the most dangerous form of skin cancer with a very poor prognosis. Melanoma develops when unrepaired DNA damage causes to skin cells to multiply and form malignant tumors. The current therapy is limited by the highly ability of this disease to metastasize rapidly. Plumbagin is a naphthoquinone (5‐hydroxy‐2‐methyl‐1, 4‐naphthoquinone), isolated from the roots of medicinal plant Plumbago zeylanica, and it is widely present in Lawsonia inermis L. It has been shown that plumbagin has an anti‐proliferative and anti‐invasive activities in various cancer cell lines; however, the anti‐cancer and anti‐metastatic effects of plumbagin are largely unknown against melanoma cells. In this study, we evaluated the effect of plumbagin on B16F10 murine melanoma cells . Plumbagin decreased B16F10 cell viability as well as the cell migration, adhesion, and invasion. The molecular mechanism was studied, and plumbagin downregulated genes relevant in MAPK pathway, matrix metalloproteinases (MMP's), and cell adhesion. Furthermore, plumbagin elevated the expression of apoptosis and tumors suppressor genes, and genes significant in reactive oxygen species (ROS) response. Taken together, our findings suggest that plumbagin has an anti‐invasion and anti‐metastasis effect on melanoma cancer cells by acting on MAPK pathway and its related genes. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0906-6705 1600-0625 |
DOI: | 10.1111/exd.14079 |