AI Article Synopsis
- Baicalein (BAI) is a flavonoid with potential therapeutic benefits against various cancers, but its effects on melanoma are not well understood.
- BAI treatment of melanoma cell lines resulted in reduced cell growth, migration, and invasion, while also inducing apoptosis, linked to changes in specific proteins and pathways.
- The study revealed that BAI inhibits melanoma progression by down-regulating colon cancer associated transcript-1 (CCAT1), which in turn impacts the Wnt/β-catenin and MEK/ERK pathways.
Article Abstract
Baicalein (BAI) is an acknowledged flavonoids compound, which is regarded as a useful therapeutic pharmaceutical for numerous cancers. However, its involvement in melanoma is largely unknown. This study aimed to examine the anti-melanoma function of BAI and unraveled the regulatory mechanism involved. A375 and SK-MEL-28 were treated with BAI for 24 h. Then, CCK-8 assay, flow cytometry, and transwell assay were carried out to investigate cell growth, migration, and invasion. RT-qPCR was applied to detect the expression of colon cancer associated transcript-1 (CCAT1) in melanoma tissues and cells. The functions of CCAT1 in melanoma cells were also evaluated. Western blot was utilized to appraise Wnt/β-catenin or MEK/ERK pathways. BAI restrained cell proliferation and stimulated cell apoptotic capability of melanoma by suppressing cleaved-caspase-3 and cleaved-PARP. Cell migratory and invasive abilities were restrained by BAI via inhibiting MMP-2 and vimentin. CCAT1 was over-expressed in melanoma tissues and down-regulated by BAI in melanoma cells. Overexpressed CCAT1 reversed the BAI-induced anti-growth, anti-migratory, and anti-invasive effects. Furthermore, BAI inhibited Wnt/β-catenin and MEK/ERK pathways-axis via regulating CCAT1. Our study indicated that BAI blocked Wnt/β-catenin and MEK/ERK pathways via regulating CCAT1, thereby inhibiting melanoma cell proliferation, migration, and invasion.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6886380 | PMC |
| http://dx.doi.org/10.1590/1414-431X20198934 | DOI Listing |
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