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Crocin promotes apoptosis of human skin cancer cells by inhibiting the JAK/STAT pathway

Pro-apoptotic effect and mechanism of crocin on skin cancer cells were investigated. After human skin cancer cells A431 and SCL-1 were processed with different concentrations of crocin in vitro (0, 0.2, 0.4, 0.8 and 1.0 mmol/l), cell viability was examined utilizing the methyl thiazolyl tetrazolium...

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Detalles Bibliográficos
Autores principales: Wang, Gongfeng, Zhang, Baofang, Wang, Yanyan, Han, Shunli, Wang, Chenghong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6257247/
https://www.ncbi.nlm.nih.gov/pubmed/30542463
http://dx.doi.org/10.3892/etm.2018.6865
Descripción
Sumario:Pro-apoptotic effect and mechanism of crocin on skin cancer cells were investigated. After human skin cancer cells A431 and SCL-1 were processed with different concentrations of crocin in vitro (0, 0.2, 0.4, 0.8 and 1.0 mmol/l), cell viability was examined utilizing the methyl thiazolyl tetrazolium assay (MTT). After 24 h incubation, the cell viability of A431 and SCL-1 decreased with increasing concentration of crocin. This indicated that crocin is capable of inhibiting the cloning ability and proliferative ability of human skin cancer cells A431 and SCL-1 in a dose-dependent manner. Flow cytometry results showed that crocin blocked A431 and SCL-1 cells in G0/G1 phase, and promoted apoptosis. The results of western blot analysis showed that the expression of Bid, procaspase-3 and ciprofloxacin in A431 and SCL-1 cells were positively correlated with crocin, while the expression of anti-apoptotic protein Bcl-2 was downregulated, which was negatively correlated with the concentration of crocin. The detection of JAK/STAT signaling pathway showed that the expression of Jak2 and Stat3 was downregulated, which was negatively correlated with crocin concentration. Crocin can significantly inhibit the proliferation of human skin cancer cells and induce cell cycle arrest in G0/G1 phase. Moreover, it can promote apoptosis of the cells. The apoptosis mechanism may be related to the downregulation of JAK/STAT pathway.