{"title":"Chelidonine inhibits melanoma cell malignancy by inactivating TLR4/NF-κB and PI3K/AKT signaling pathways.","authors":"Yu Zhou, Han Han, Peng Li, Wei Wei","doi":"10.4196/kjpp.24.383","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"509-5159"},"PeriodicalIF":2.2000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198443/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Korean Journal of Physiology & Pharmacology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.4196/kjpp.24.383","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/4/11 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}
引用次数: 0
Abstract
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.
期刊介绍:
The Korean Journal of Physiology & Pharmacology (Korean J. Physiol. Pharmacol., KJPP) is the official journal of both the Korean Physiological Society (KPS) and the Korean Society of Pharmacology (KSP). The journal launched in 1997 and is published bi-monthly in English. KJPP publishes original, peer-reviewed, scientific research-based articles that report successful advances in physiology and pharmacology. KJPP welcomes the submission of all original research articles in the field of physiology and pharmacology, especially the new and innovative findings. The scope of researches includes the action mechanism, pharmacological effect, utilization, and interaction of chemicals with biological system as well as the development of new drug targets. Theoretical articles that use computational models for further understanding of the physiological or pharmacological processes are also welcomed. Investigative translational research articles on human disease with an emphasis on physiology or pharmacology are also invited. KJPP does not publish work on the actions of crude biological extracts of either unknown chemical composition (e.g. unpurified and unvalidated) or unknown concentration. Reviews are normally commissioned, but consideration will be given to unsolicited contributions. All papers accepted for publication in KJPP will appear simultaneously in the printed Journal and online.