Lasalocid inhibits melanoma by down-regulating FOXM1 through PI3K/AKT and JNK/P38 MAPK pathways

拉沙洛西通过 PI3K/AKT 和 JNK/P38 MAPK 通路下调 FOXM1 来抑制黑色素瘤

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作者:Qiang Yuan, Hangyu Jiang, Maofei Zhu, Yueming Chu, Yan Zhang, Jun Bie, Lin Li

Abstract

Melanoma poses a significant challenge to patients due to its aggressive nature and limited treatment options. Recent studies have suggested that lasalocid, a feed additive ionophore antibiotic, may have potential as an anticancer agent. However, the mechanism of lasalocid in melanoma is unclear. This study found that lasalocid could inhibit melanoma cell proliferation, migration, and invasion, while inducing cell cycle arrest and apoptosis. Transcriptome sequencing and bioinformatics analysis identified FOXM1 as the hub gene of lasalocid-mediated melanoma treatment. In vitro experiments confirmed that lasalocid regulates FOXM1 expression through the PI3K/AKT and JNK/P38 MAPK pathways. In vivo experiments showed that lasalocid effectively inhibited melanoma growth with acceptable safety. In summary, our study results emphasize lasalocid's potential as a melanoma therapeutic agent and elucidate its role in regulating FOXM1 through the PI3K/AKT and JNK/P38 MAPK pathways.

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