Chelidonine inhibits melanoma cell malignancy by inactivating TLR4/NF-κB and PI3K/AKT signaling pathways.

Melanoma is a common and aggressive tumor, characterized by a high incidence rate and extensive metastasis. Chelidonine exhibits a broad range of biological properties including anti-inflammatory, antimicrobial, and anticancer effects. Our study is intended to explore the effects chelidonine of on melanoma cells. In detail, CCK-8 assay was used for detection of cell viability. The colony formation assay was carried out to measure cell proliferation. Wound healing assay and Transwell assay were employed to evaluate cell migration and invasion, respectively. Cell apoptosis was determined by flow cytometry analysis, and protein level was measured by Western blotting. The experimental results demonstrated that chelidonine treatment inhibited cell viability and cell proliferation but facilitated cell apoptosis of melanoma cells. Besides, chelidonine suppressed melanoma cancer cell migration and invasion by attenuating epithelial-mesenchymal transition process. Moreover, chelidonine inhibited the activation of TLR4/NF-κB and PI3K/AKT pathways by downregulation of the protein level of TLR4, phosphorylated p65, phosphorylated PI3K, and phosphorylated AKT in melanoma cells. Furthermore, TAK-242 or LY294002 further enhanced the inhibitory effects chelidonine of on malignant cell behavior. In conclusion, our findings demonstrate that chelidonine effectively suppresses the malignancy of melanoma cells through the inhibition of TLR4/NF-κB and PI3K/AKT signaling pathways, suggesting its potential as a promising therapeutic agent for melanoma treatment.