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Ginkgetin Inhibits the Growth of Melanoma Cells by Regulating JAK2/STAT3 Signaling Pathway

Authors: Chuchen Zhuang; Liping Zhang;

Ginkgetin Inhibits the Growth of Melanoma Cells by Regulating JAK2/STAT3 Signaling Pathway

Abstract

Melanoma is the most invasive skin cancer with the highest risk of death. Better understanding of the pathogenesis of melanoma has helped identify new therapeutic targets and drugs against melanoma in prolonging the survival of melanoma patients. Ginkgetin is a bioflavonoid compound extracted from the leaves of Ginkgo biloba, which exhibits a multitude of biological activities such as antiviral, antioxidant, anti-inflammatory, and antifungal. Although it has been shown to suppress the progression of multiple types of tumors, its role in melanoma remains unexplored. Therefore, we investigated the role and potential mechanism of ginkgetin in melanoma. The results of the studies reported here show that ginkgetin inhibits proliferation and promotes apoptosis of the melanoma cell lines. Ginkgetin also induces G1/G0 arrest of the melanoma cells by regulating signal transducer and activator of transcription 3 and mitogen-activated protein kinase signaling pathways. We therefore believe that ginkgetin may be a promising drug in the treatment and cure of melanoma.

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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
1
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Average
Average