ArticleScientific reports2017
Inhibiting STAT3 signaling is involved in the anti-melanoma effects of a herbal formula comprising Sophorae Flos and Lonicerae Japonicae Flos.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Antimelanoma potential of natural compounds derived from plants: a systematic review of in vivo studies of B16 melanoma and its sublines.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025Pooled it
- Arnicolide D: a multi-targeted anticancer sesquiterpene lactone-preclinical efficacy and mechanistic insights.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Review
- Dexamethasone and OLT1177 Cooperate in the Reduction of Melanoma Growth by Inhibiting STAT3 Functions.Cells · 2023Article
- Flos puerariae ameliorates the intestinal inflammation ofFrontiers in pharmacology · 2022Article
- Activation of STAT3 is a key event in TLR4 signaling-mediated melanoma progression.Cell death & disease · 2020Article
- Inhibiting the Src/STAT3 signaling pathway contributes to the anti-melanoma mechanisms of dioscin.Oncology letters · 2020Article
- Advances in Molecular Mechanisms for Traditional Chinese Medicine Actions in Regulating Tumor Immune Responses.Frontiers in pharmacology · 2020Review
- STAT3 and STAT5 Targeting for Simultaneous Management of Melanoma and Autoimmune Diseases.Cancers · 2019Review
- Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A herbal formula (SL) comprising Sophorae Flos and Lonicerae Japonicae Flos was traditionally used to treat melanoma. Constitutively active signal transducer and activator of transcription 3 (STAT3) has been proposed as a therapeutic target in melanoma. Here we investigated whether an ethanolic extract of SL (SLE) exerted anti-melanoma activities by inhibiting STAT3 signaling. B16F10 allograft model, A375 and B16F10 cells were employed to assess the in vivo and in vitro anti-melanoma activities of SLE. A375 cells stably expressing STAT3C, a constitutively active STAT3 mutant, were used to determine the role of STAT3 signaling in SLE's anti-melanoma effects. Intragastric administration of SLE (1.2 g/kg) potently inhibited melanoma growth in mice and inhibited STAT3 phosphorylation in the tumors. In cultured cells, SLE dramatically reduced cell viability, induced apoptosis, suppressed migration and invasion, and restrained STAT3 activation and nuclear localization. STAT3C overexpression in A375 cells diminished SLE's effects on cell viability, apoptosis and invasion. Collectively, SLE exerted potent anti-melanoma effects partially by inhibiting STAT3 signaling. This study provides pharmacological justification for the traditional use of this formula in treating melanoma, and suggests that SLE has the potential to be developed as a modern alternative and/or complimentary agent for melanoma treatment and prevention.
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